Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Topical acyclovir speeds healing and decreases viral shedding and pain in immunocompromised patients with chronic, ulcerative herpetic lesions; it may be used when one does not wish to add another systemic drug. In severe first-episode and life-threatening infections, acyclovir may be administered intravenously for 7 to 10 days. In milder and non-life-threatening first-episode infections, acyclovir may be given orally in a dosage of 200 mg five times a day for 10 days. With these doses, healing is 50% faster and viral shedding stops 90% sooner. Acyclovir given early during first-episode infections, especially true primary infections, may decrease immune responses to the virus, but these usually become normal later. Fewer than six recurrences a year may be managed by 200 mg acyclovir orally five times a day for 5 days beginning as soon as symptoms appear. More than six recurrences a year, often every month, may be managed by continuous suppressive oral acyclovir therapy. Kaposi's varicelliform eruption responds to acyclovir given orally or intravenously depending on circumstances. Primary and recurrent herpetic whitlow respond to acyclovir.
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PMID:Treatment of mucocutaneous herpes simplex infections with acyclovir. 333 39

Out of 80 kidney graft recipients treated with cyclosporin A and low dose steroids 19 (23.8%) developed herpes virus infection and from these 15 (18.8%) herpetic stomatitis. Evaluation of enhancing factors for herpetic stomatitis suggested a role of cyclosporin A rather than of steroids and a probable relation to preceding CMV infection. Acyclovir treatment was effective on the course of stomatitis and pain in 12 of the 15 patients. No serious side effects were observed. Leukopenia as a possible hazard was discussed.
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PMID:Herpetic stomatitis and acyclovir therapy in cyclosporin A treated renal graft recipients. 391 58

Sixty-three immunocompromised patients with infections caused by herpes simplex virus were evaluated in a double-blind, placebo-controlled study of topical acyclovir therapy; 33 patients received acyclovir and 30 received the placebo. The two populations of patients were balanced in terms of age, race, sex, underlying disease, preceding chemotherapy, and site, size, and duration of lesions. Acyclovir recipients experienced an acceleration in the clearance of virus (P = .0006), the resolution of pain (P = .004), and the total healing of lesions (P = .038); median temporal differences between populations averaged six days for each of these three parameters. The surface area of herpetic lesions continued to enlarge in placebo recipients after entry into the trial; in contrast, lesion surface area decreased progressively during therapy in drug recipients. The speed of healing was influenced by lesion size. Patients with lesions of greater than or equal to 50 mm2 benefited most from therapy, particularly in terms of pain resolution and time to total healing (median differences between groups, eight days). Irrespective of underlying disease, sex, preceding chemotherapy, or age, acyclovir therapy was of clinical benefit. No adverse clinical or laboratory reactions were encountered.
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PMID:Infections caused by herpes simplex virus in the immunocompromised host: natural history and topical acyclovir therapy. 609 May 39

11 of 24 immunocompromised patients with mucocutaneous herpes simplex virus (HSV) infections were given intravenous acyclovir in a randomised double-blind placebo-controlled study. Patients receiving acyclovir experienced no major adverse effects. The median times to cessation of new lesion formation, lesion crusting, lesion healing, cessation of pain, and termination of viral shedding were shorter in the acyclovir-treated group than in the placebo group. The time-to-event probability curves for the acyclovir and placebo groups were significantly different for cessation of pain (p=0.032) and termination of viral shedding (p=0.004). The median times to termination of viral shedding were also statistically different (p=0.045). Acyclovir seems to be a non-toxic and effective treatment for mucocutaneous HSV infections in immunocompromised patients.
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PMID:Acyclovir therapy for mucocutaneous herpes simplex infections in immunocompromised patients. 611 52

31 adults took part in a randomised, placebo-controlled, double-blind trial of intravenous acyclovir therapy (500 mg/m2 intravenously 3 times daily for 5 days) for acute herpes zoster. Acyclovir reduced pain, decreased erythema, prevented the formation of new lesions, and healed skin faster than did placebo. The duration of viral shedding was also significantly shorter in acyclovir recipients (2 days versus 5 days). However, 6(35%) of 17 acyclovir recipients had recurrence of pain after the drug was discontinued, and acyclovir did not appear to affect post-herpetic neuralgia. Acyclovir therapy was associated with a transient rise in serum creatinine levels, and may have been related to nausea and vomiting. Intravenous acyclovir was effective therapy for acute herpes zoster but the ideal treatment regimen might be a lower daily dose given for a longer period.
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PMID:Acyclovir therapy for acute herpes zoster. 612 37

Acyclovir (acycloguanosine) is a new antiviral compound with activity against certain herpes viruses. Acyclovir is phosphorylated preferentially in virus-infected cells into its active form, acyclovir triphosphate, an inhibitor of viral-induced DNA polymerase. Acyclovir, which possesses an acyclic carbohydrate moiety, also causes premature DNA chain termination. Acyclovir has shown clinical activity against herpes simplex virus (HSV) types 1 and 2 and varicella zoster virus (VZV), but its usefulness in cytomegalovirus, Epstein-Barr virus, and chronic hepatitis B infections requires further study. In randomized clinical trials of infections caused by HSV and VZV, intravenous acyclovir has been shown to shorten the duration of viral shedding and lesion pain and hasten the resolution of skin lesions, with minimal toxicity.
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PMID:The clinical use of intravenous acyclovir. 631 3

In a randomized, placebo-controlled, double-blind trial of intravenous acyclovir in the treatment of varicella zoster virus (VZV) infections, 8 of 20 immunocompromised children with varicella received acyclovir (500 mg/m2/dose three times daily for 7 days). There was no significant difference in skin healing between the acyclovir and placebo groups although there was a significant reduction in the incidence of development of pulmonary involvement during acyclovir treatment. Nineteen out of 34 patients received vidarabine (10 mg/kg/day for 5 days). Vidarabine significantly shortened the duration of new vesicle formation. Both drugs significantly reduced the incidence of visceral varicella, the most serious complication of VZV infection. An open trial also concluded that early treatment of varicella in these patients is essential. Of the 94 patients with zoster infection, 52 received acyclovir (500 mg/m2/dose infused over one hour three times daily for 7 days). Acyclovir recipients healed more rapidly, had fewer days of pain and shorter duration of viral shedding compared with placebo patients. The most important finding was that acyclovir significantly protected against progression of zoster as defined by development or progression of cutaneous dissemination and development of visceral zoster. Vidarabine seemed to be equally effective in this respect. The likelihood of cutaneous dissemination is related to the nature of the underlying condition. The in vitro sensitivity of VZV isolates from patients with second episode VZV infection during the trial did not change appreciably which suggests that VZV does not become resistant to acyclovir during therapy.
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PMID:Acyclovir therapy of varicella-zoster virus infections in immunocompromised patients. 631 96

Acyclovir (aciclovir) is a nucleoside analogue antiviral drug related to cytarabine, idoxuridine, trifluridine and vidarabine. In common with these earlier antivirals, acyclovir is active against some members of the herpesvirus group of DNA viruses. The efficacy of topical acyclovir has been convincingly demonstrated in ocular herpetic keratitis, and in initial and primary initial genital herpes infection, but little or no clinical benefit was seen when non-primary initial genital infections were assessed separately. Acyclovir ointment demonstrated little benefit in recurrent genital herpes but topical acyclovir cream decreased the course of the infection by 1 to 2 days. Orally and intravenously administered acyclovir were beneficial in initial genital herpes infections, and oral therapy shortened the duration of recurrent infections by 1 to 2 days but did not ameliorate pain. In non-immunocompromised patients with recurrent herpes simplex labialis, generally little clinical benefit was seen with the use of topical acyclovir ointment even when therapy was initiated during the prodromal phase, while topical acyclovir cream effected small but significant improvements in the clinical but not the symptomological course of the disease. However, in immunocompromised patients, both intravenous and topical acyclovir shortened the clinical course of herpes simplex virus infections occurring mainly on the lips, oral mucosa and face, and prophylaxis with either oral or intravenous acyclovir suppressed the appearance of recurrent lesions from latent virus for the period of drug administration, but acyclovir did not eradicate latent herpesviruses. In non-immunocompromised patients, intravenous acyclovir was shown to decrease the acute pain of zoster, especially in the elderly, but postherpetic neuralgia was not ameliorated. When immunocompromised patients were studied, intravenous acyclovir inhibited the progression of zoster infections and shortened the healing time and duration of viral shedding in patients with cutaneous disseminated zoster. However, acute and post-herpetic pain were not significantly affected. Well designed controlled studies are underway to establish the efficacy of acyclovir in herpes simplex encephalitis and cytomegalovirus infections in immunocompromised patients, infections due to Epstein-Barr virus, and neonatal herpesvirus infections. Despite some aspects of the drug's use which require further clarification, acyclovir will make a major impact on the treatment of herpesviral infections. Barring unexpected findings with wider clinical use, it will become the agent of choice in several conditions.
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PMID:Acyclovir. A review of its pharmacodynamic properties and therapeutic efficacy. 631 32

In a double-blind randomised placebo-controlled trial of topical acyclovir in initial (first episode) genital herpes 18 patients received acyclovir ointment and 22 matching placebo ointment. Acyclovir significantly reduced the duration of viral shedding from external and all genital lesions, the duration of vesicles, the time to crusting, the time to complete healing of external and all genital lesions, new lesion formation, and the duration of pain, itching, and all symptoms combined for all patients. In female patients alone the time to crusting was not significantly different and the duration of pain only approached significance but the effects were otherwise the same as for all patients. No patients reported any adverse effects of treatment. Topical acyclovir is well tolerated and effective in treating initial genital herpes.
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PMID:Topical acyclovir in the treatment of initial genital herpes. 633 97

We performed a double-blind placebo-controlled trial of oral acyclovir in the treatment of first episodes of genital herpes simplex virus infections in 48 young adults (31 women and 17 men). Subjects were randomized to receive either placebo or acyclovir (200 mg per dose) five times daily for 10 days; they were examined on at least eight visits until healed and at monthly visits thereafter. Acyclovir treatment, as compared with placebo, significantly reduced virus shedding, new lesion formation after 48 hours, and the duration of genital lesions in both men and women. The total duration and severity of clinical symptoms (such as pain, adenopathy, dysuria, and malaise) were significantly reduced by acyclovir in both men and women by the third and fourth day, respectively (P less than or equal to 0.025), as compared with placebo. No toxicity was observed. Recurrence rates have so far been similar in placebo and acyclovir recipients. Oral acyclovir treatment of first-episode genital herpes simplex virus infections is clinically effective, but it does not seem to prevent virus latency or associated recurrent disease.
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PMID:Treatment of first episodes of genital herpes simplex virus infection with oral acyclovir. A randomized double-blind controlled trial in normal subjects. 633 23


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