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herpes zoster/protease
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Alterations in mast cell proteinases and protease inhibitors in the progress of cutaneous herpes zoster infection.
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The possible involvement of mast cell proteases in the cutaneous inflammation of herpes zoster was studied histochemically in ten patients. Mast cell tryptase and chymase bioactivities were demonstrated enzyme-histochemically. The localization of protease inhibitors as well as tryptase and chymase
High incidence of herpes zoster in patients with AIDS soon after therapy with protease inhibitors.
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A high incidence of herpes zoster was noticed among patients with AIDS, shortly after addition of a protease inhibitor to their baseline treatment with nucleoside analogue reverse-transcriptase inhibitors. Within a median follow-up of 64 weeks (range, 34-103 weeks), 14 patients (7%) had a first
Herpes zoster as an immune restoration disease in AIDS patients during therapy including protease inhibitors.
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A prospective study to evaluate the incidence of herpes zoster (HZ) as an immune restoration disease in patients with AIDS during highly active antiretroviral therapy (HAART) was conducted in a series of 115 patients diagnosed with AIDS initiated on HAART between 1 January 2000 and 31 July 2001. Of
[Secondary prophylaxis for herpes zoster wi oral acyclovir in HIV patients].
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We studied 39 AIDS patients from 1989 to 1996, with previous history of herpes zoster. Twelve of them received acyclovir (ACV) secondary prophylaxis. There were 31 males and 8 females, mean age 33.9 years (19-60) during first herpes zoster. Transmission was sexual in 71.8%. Among these 39 patients,
Predictive factors of herpes zoster HIV-infected patients: another adverse effect of crack cocaine.
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A retrospective cohort study was conducted on 1541 HIV-infected patients to determine variables associated with the incidence of herpes zoster. A single failure Cox model showed that herpes zoster incidence increased following the first 6 months of antiretroviral treatment adjusted hazard ratio
Crystal structure of varicella-zoster virus protease.
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Varicella-zoster virus (VZV), an alpha-herpes virus, is the causative agent of chickenpox, shingles, and postherpetic neuralgia. The three-dimensional crystal structure of the serine protease from VZV has been determined at 3.0-A resolution. The VZV protease is essential for the life cycle of the
Boceprevir-induced Herpes Zoster.
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Herpes zoster is caused by reactivation of the varicella zoster virus (VZV), that attacks peripheral or cranial nerves and result in painful cutaneous inflammation. Boceprevir is a protease inhibitor which used as a new therapeutic agent for chronic hepatitis C infection. Boceprevir associated
Incidence and risk factors of herpes zoster among hiv-positive patients in the german competence network for HIV/AIDS (KompNet): a cohort study analysis.
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BACKGROUND
HIV infection is a risk factor for the development of Herpes zoster (HZ) and its complications. Prior to antiretroviral therapy (ART), HZ incidence in HIV-infected individuals ranged from 2.9-5.1/100 person-years. There is limited evidence for the impact of ART on HZ occurrence among
Carbamazepine--indinavir interaction causes antiretroviral therapy failure.
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OBJECTIVE
To report a case of antiretroviral therapy failure caused by an interaction between carbamazepine and indinavir.
METHODS
A 48-year-old HIV-positive white man was treated with antiretroviral triple therapy, consisting of indinavir, zidovudine, and lamivudine. His HIV-RNA (viral load) became
Successful treatment of refractory postherpetic neuralgia with topical gallium maltolate: case report.
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BACKGROUND
Postherpetic neuralgia is a common sequela of herpes zoster (shingles), in which chronic pain may last for weeks to years. Currently, available treatments include systemic opioid analgesics, tricyclic antidepressants, corticosteroids, and anticonvulsants, as well as topical capsaicin and
Dermatologic adverse effects of antiretroviral therapy: recognition and management.
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Despite the decrease in opportunistic infections associated with HIV in the highly active antiretroviral treatment (HAART) era, a significant number of patients still present with skin pathology, some of which can be attributed directly or indirectly to antiretroviral therapy. The non-nucleoside
Viral and immunologic follow up of 4 to 9 years of AIDS treatments by quadruple combinations of virostatics including integrase inhibitors applied in short sequences differing by drug rotation.
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OBJECTIVE
To present the 4 to 9 years (median: 6 years) treatment follow up of 10 HIV1-AIDS patients, 9 at AIDS and 1 at A3 stages.
METHODS
We have applied from 1992 to 1994, AZT combined with 2 integrase inhibitors, acriflavine and hydroxy-methyl-ellipticine. We could shift, in 1994, to
Treatment modalities for patients with HIV disease.
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Pharmacologic and psychosocial interventions begin at the time HIV infection is diagnosed and continue to the end of the patient's life. It is important that the nurse and patient communicate effectively with one another about the significance of being HIV positive, including disease progression and
Suction blister formation in skin after acute and repeated mast cell degranulation.
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Mast cells and their proteases are thought to participate in the development of skin blisters in various pathological conditions. In this study, suction blistering was used as an experimental model to evaluate the significance of mast cells in blister formation after pre-treatment of normal skin
Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood.
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Therapy with oral proteolytic enzymes (OET) with combination drug products containing papain, bromelain, trypsin, and chymotrypsin has been shown to be beneficial in clinical settings such as radiotherapy-induced fibrosis, bleomycin pneumotoxicity and immunosuppression in cancer, all of which are
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