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Treatment for herpes zoster, natural remedies for herpes simplex skin rash - For You

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Herpes zoster infection (shingles) results from the reactivation of varicella zoster virus infection.
The rash develops from maculopapular lesions forming a beltlike pattern on the patient's trunk, but the band of rash may appear anywhere on the body including the eyes. The main symptom associated with postherpetic neuralgia is pain, which persists for a long period beyond the resolution of the shingles rash.
In excess of 60% of people older than 60 years, especially those with diminished immunity due to diabetes and cancers, are afflicted by herpes zoster. Prednisone use in conjunction with acyclovir resulted in the reduction of the pain associated with acute herpes zoster. Lidocaine is an amide-type local anesthetic agent that stabilizes neuronal membranes by inhibiting the ionic fluxes required for the initiation and conduction of impulses.
The outcome of treatment of shingles is often unsatisfactory, although the antiviral medications reduce the duration of pain during the acute phase but do not prevent PHN complications and pain.
Initially, the host is able to produce varicella zoster virus—specific, cell-mediated immunity during the infection.
Low levels of immune globulin have been shown to predispose patients to recurring herpes zoster infection. Despite the usefulness of prednisone in managing the associated pain with herpes zoster infection, it has not been shown to decrease or prevent the incidence of PHN. I believe it is a neurologic condition and that it should be aggressively treated with some kind of physiologic treatments by a neurologist. Postherpetic neuralgia is very resistant to treatment and results in decreased quality of life.

Periodically, endogenous and exogenous boosting of the immunity against varicella results in the virus remaining dormant for decades. Pain is the primary complaint with active-stage shingles and the symptom for which patients seek medical care. The need for regular application of capsaicin must be emphasized to patients to maintain pain relief. The parenteral route is available for patients who are unable to utilize the oral dosing route. Lidocaine-containing patches significantly reduce pain intensity throughout the dosing interval for up to 12 hours. The CDC Advisory Committee on Immunization Practices recommends routine vaccination of all persons age >60 years with one dose of zoster vaccine. Occasionally, zoster can cause motor weakness in noncranial nerve distributions, calledzoster paresis.
The pain is stipulated to be due to persistent C-fiber nociceptor activity in the nerve cells, although studies have shown chronic neural loss and scarring in nerves affected by herpes zoster injury. It is important to educate patients on the need for thorough hand washing after each application of capsaicin. Lidocaine patches were superior to both no treatment and vehicle patches in averaged category pain relief scores. Combining TCAs with antiviral drugs during herpes zoster infection has been shown to decrease the intensity of PHN pain but does not prevent it.
One specific risk for patients who are immunocompromised is dissemination of the zoster rash.

Zoster vaccination is not indicated to treat acute zoster, to prevent persons with acute zoster from developing PHN, or to treat ongoing PHN. Cutaneous dissemination generally occurs only among immunocompromised patients, occurring in up to 37% of zoster cases in the absence of antiviral treatment. Valacyclovir appears to be more efficacious in decreasing the severity of pain associated with acute herpes zoster and the duration of the PHN when compared to acyclovir. Before routine administration of zoster vaccine, it is not necessary to ask patients about their history of varicella (chickenpox) or to conduct serologic testing for varicella immunity. While cutaneous dissemination is not life-threatening, it is a marker for potential virus seeding of the lungs, liver, gut, and brain and can cause pneumonia, hepatitis, encephalitis, and disseminated intravascular coagulopathy in 10% to 50% of episodes. Rarely, patients will experience acute focal neurologic deficits weeks to months after resolution of the zoster rash, involving the trigeminal distribution contralateral to the initial rash. When antiviral therapy starts within 72 hours of the onset of herpes zoster, acyclovir, valacyclovir, and famciclovir have been shown to significantly shorten the periods of acute pain, virus shedding, rash, and acute and late-onset complications. Other rare neurologic complications of herpes zoster include myelitis, aseptic meningitis, and meningoencephalitis. The risk for neurologic zoster complications is generally increased in immunocompromised persons.

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