Shingles: Difference between revisions
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===Antiviral drugs=== |
===Antiviral drugs=== |
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[[Aciclovir|Acyclovir]] (an [[antiviral drug]]) inhibits replication of the viral DNA, and is used both as [[prophylaxis]] (''e.g.'', in patients with [[AIDS]]) and as therapy for herpes zoster. Other antivirals are [[valacyclovir]] and [[famciclovir]]. During the [[Acute (medical)|acute phase]], oral acyclovir should be given. Use of acylovir is most effective, if started within 24 to 72 hours of the onset of symptoms, so medical care should be obtained as soon as the condition is recognized. |
[[Aciclovir|Acyclovir]] (an [[antiviral drug]]) inhibits replication of the viral DNA, and is used both as [[prophylaxis]] (''e.g.'', in patients with [[AIDS]]) and as therapy for herpes zoster. Other antivirals are [[valacyclovir]] and [[famciclovir]]. During the [[Acute (medical)|acute phase]], oral acyclovir should be given. Use of acylovir is most effective in moderating the progress of the symptoms, and in preventing post-herpetic neuralgia, if started within 24 to 72 hours of the onset of symptoms, so medical care should be obtained as soon as the condition is recognized. [[Immunocompromised]] patients may respond best to intravenous acyclovir. In patients who are at high risk for recurrences, an oral dose of acyclovir, taken twice daily, is usually effective.<ref name="Johnson"/> It is also reported that the [[amino acid]] [[lysine]] inhibits the replication of herpes zoster.<ref>{{cite journal|last=Griffith|first=RS|coauthors=Walsh DE, Myrmel KH, Thmpson RW, and Behforooz A|title=Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis|journal=Dermatologica|date=1987|volume=175|issue=4|pages=183-190|id=PMID 3115841}}</ref> |
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Where they can be accessed and in time, antiviral drugs such as acyclovir are the treatment of choice, with most evidence for ameliorating the progress of symptoms in shingles (herpes zoster), and may have a limited effect on the development of post herpetic neuralgia (PHN).” <ref>{{cite web |url=http://www.ihmf.org/guidelines/Zoster-Associated%20Pain%20What%20is%20Known,%20Who%20is%20at%20Risk%20and%20How%20Can%20it%20be%20Managed.pdf|title= “Zoster-Associated Pain: What is Known, Who is at Risk and How can it be Managed?” |author= Johnson R|authorlink= |coauthors= |date= |format= |work= Statements and Recommendations|publisher= International Herpes Management Forum|pages=page 3|language= English|archiveurl= |archivedate= |quote=}}</ref> <ref name="pmid17177766">{{cite journal |author=Niv D, Maltsman-Tseikhin A |title=Postherpetic neuralgia: the never-ending challenge |journal=Pain practice : the official journal of World Institute of Pain |volume=5 |issue=4 |pages=327-40 |year=2005 |pmid=17177766 |doi=10.1111/j.1533-2500.2005.00035.x}}</ref> <ref name="pmid10735485">{{cite journal |author=Alper BS, Lewis PR |title=Does treatment of acute herpes zoster prevent or shorten postherpetic neuralgia? |journal=The Journal of family practice |volume=49 |issue=3 |pages=255-64 |year=2000 |pmid= 10735485 |accessdate=2007-06-10 |doi=}}</ref> |
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[[Immunocompromised]] patients may respond best to intravenous acyclovir. In patients who are at high risk for recurrences, an oral dose of acyclovir, taken twice daily, is usually effective.<ref name="Johnson"/> It is also reported that the [[amino acid]] [[lysine]] inhibits the replication of herpes zoster.<ref>{{cite journal|last=Griffith|first=RS|coauthors=Walsh DE, Myrmel KH, Thmpson RW, and Behforooz A|title=Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis|journal=Dermatologica|date=1987|volume=175|issue=4|pages=183-190|id=PMID 3115841}}</ref> |
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===Other drugs=== |
===Other drugs=== |
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The long term complication of herpes zoster is, Post Herpetic Neuralgia which may cause persistent pain that lasts for years. Pain management is difficult and conventional treatment may be ineffective. Alternative agents to [[analgesics]] may be tried, by your doctor, including [[tricyclic antidepressants]] in small doses (particularly [[amitriptyline]]), [[anticonvulsants]] (e.g. [[gabapentin]]), oral corticosteroids, lidocaine patch, opiods and/or topical [[capsaicin]]. Intrathecal methylprednisolone may be used in selected patients with persistent pain. Over-the-counter topical anesthetics may reduce pain associated with the disease. However it should be realised there is only limited clinical evidence to support such use of aspirin, acetaminophen/paracetamol, non-steroidal anti-inflammatory drugs, ( NSAIDs), opioid analgesics (including tramadol), tricyclic antidepressants (especially nortriptyline), and anticonvulsants (gabapentin and pregabalin) <ref>{{cite web |url=http://www.ihmf.org/guidelines/Zoster-Associated%20Pain%20What%20is%20Known,%20Who%20is%20at%20Risk%20and%20How%20Can%20it%20be%20Managed.pdf | title= “Zoster-Associated Pain: What is Known, Who is at Risk and How can it be Managed?”|accessdate=2007-06-10 |author= Johnson R|authorlink= |coauthors= |date= |format= |work= Statements and Recommendations|publisher= International Herpes Management Forum|pages=page 3|language= English|archiveurl= |archivedate= |quote=}}</ref> <ref name="pmid17143845">{{cite journal |author=Dworkin RH, Johnson RW, Breuer J, ''et al'' |title=Recommendations for the management of herpes zoster |journal=Clin. Infect. Dis. |volume=44 Suppl 1 |issue= |pages=S1-26 |year=2007 |pmid=17143845 |doi=10.1086/510206}}</ref> |
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Medications are available to ameliorate the pain of PHN, but data suggests these agents provide incomplete pain relief and their use is often accompanied by troubling side effects, especially in the populations of the aged and immuno-compromised, who should be monitored closely.<ref>{{cite web | url = http://www.jaoa.org/cgi/content/full/107/suppl_1/S2 | title = The Burden of Herpes Zoster and Postherpetic Neuralgia in the United States -- Weaver 107 (Supplement 1): S2 -- Journal of the American Osteopathic Association | accessdate = 2007-06-16 | format = | work = }}</ref> <ref>{{cite web |url=http://www.jfponline.com/Pages.asp?AID=2465&UID= |title=The Journal of Family Practice |accessdate=2007-06-16 |format= |work=}}</ref><ref name="pmid12676845">{{cite journal |author=Johnson RW, Dworkin RH |title=Treatment of herpes zoster and postherpetic neuralgia |journal=BMJ |volume=326 |issue=7392 |pages=748-50 |year=2003 |pmid=12676845 |doi=10.1136/bmj.326.7392.748}}</ref> |
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[[Cimetidine]], a common component of over-the-counter heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances.<ref>{{cite journal|author=Kapinska-Mrowiecka M, &Toruwski G | title=Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation. | journal= Pol Tyg Lek. | year=1996. | pages=338-339 | volume=51 | issue=23-26 | id=PMID 9273526}}</ref><ref>{{cite journal|author=Hayne ST, & Mercer JB|title=Herpes zoster: treatment with cemetidine|journal=Canadian Medical Association Journal|year=1983|pages=1284-1285| volume=129|issue=12|id=PMID 6652595}}</ref><ref>{{cite journal|author=Notmann J, Arieli J, Hart J, Levinsky H, Halbrecht I, & Sendovsky U | title=In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine. | journal=Asian Pacific Journal Allergy and Immunology|year=1994|pages=51-58|volume=12|issue=1|id=PMID 7872992}}</ref> This usage is considered an [[off-label use]] of the drug. In addition, cimetidine and [[probenecid]] have been shown to reduce the renal clearance of aciclovir. <ref>{{cite journal|author=De Bony F, Tod M, Bidault R, On NT, Posner J, & Rolan P| title=Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir |journal=Antimicrobial Agents and Chemotherapy|year=2002|pages=458-463|volume=46 |issue=2|id=PMID 11796358}}</ref> The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of acyclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician. |
[[Cimetidine]], a common component of over-the-counter heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances.<ref>{{cite journal|author=Kapinska-Mrowiecka M, &Toruwski G | title=Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation. | journal= Pol Tyg Lek. | year=1996. | pages=338-339 | volume=51 | issue=23-26 | id=PMID 9273526}}</ref><ref>{{cite journal|author=Hayne ST, & Mercer JB|title=Herpes zoster: treatment with cemetidine|journal=Canadian Medical Association Journal|year=1983|pages=1284-1285| volume=129|issue=12|id=PMID 6652595}}</ref><ref>{{cite journal|author=Notmann J, Arieli J, Hart J, Levinsky H, Halbrecht I, & Sendovsky U | title=In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine. | journal=Asian Pacific Journal Allergy and Immunology|year=1994|pages=51-58|volume=12|issue=1|id=PMID 7872992}}</ref> This usage is considered an [[off-label use]] of the drug. In addition, cimetidine and [[probenecid]] have been shown to reduce the renal clearance of aciclovir. <ref>{{cite journal|author=De Bony F, Tod M, Bidault R, On NT, Posner J, & Rolan P| title=Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir |journal=Antimicrobial Agents and Chemotherapy|year=2002|pages=458-463|volume=46 |issue=2|id=PMID 11796358}}</ref> The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of acyclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician. |
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===Complementary Therapies=== |
===Complementary Therapies=== |
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Digestive Enzymes, are available on script and in some over the counter preparations. Before the availability of antivirals, oral pancreatic enzyme therapy in shingles was used in some countries and later subjected to clinical and scientific research. A large scale multi-centre clinical study, using an oral |
Digestive Enzymes, are available on script and in some over the counter preparations. Before the availability of antivirals, oral pancreatic enzyme therapy in shingles was used in some countries and later subjected to clinical and scientific research. A large scale multi-centre clinical study, using an oral preparation of such enzymes, has shown promising results.<ref name="pmid7713467">{{cite journal |author=Billigmann P |title=[Enzyme therapy--an alternative in treatment of herpes zoster. A controlled study of 192 patients] |language=German |journal=Fortschr. Med. |volume=113 |issue=4 |pages=43-8 |year=1995 |pmid=7713467 |doi=}}</ref> <ref name="pmid16813460">{{cite journal |author=Roxas M |title=Herpes zoster and postherpetic neuralgia: diagnosis and therapeutic considerations |journal=Alternative medicine review : a journal of clinical therapeutic |volume=11 |issue=2 |pages=102-13 |year=2006 |pmid=16813460 |doi=}}</ref> The results of another clinical study support the concept that oral enzyme therapy is beneficial in diseases characterized in part by TGF-beta overproduction that included shingles patients. <ref name="pmid11561866">{{cite journal |author=Desser L, Holomanova D, Zavadova E, Pavelka K, Mohr T, Herbacek I |title=Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood |journal=Cancer Chemother. Pharmacol. |volume=47 Suppl |issue= |pages=S10-5 |year=2001 |pmid=11561866 |doi=}}</ref> TGF-B has also been found higher in instances of VZV <ref name="pmid15547808">{{cite journal |author=Kaygusuz I, Gödekmerdan A, Keleş E, ''et al'' |title=The role of viruses in idiopathic peripheral facial palsy and cellular immune response |journal=American journal of otolaryngology |volume=25 |issue=6 |pages=401-6 |year=2004 |pmid=15547808 |doi=}}</ref> <ref name="pmid11094200">{{cite journal |author=Sato M, Abe T, Tamai M |title=Expression of the Varicella Zoster Virus Thymidine Kinase and Cytokines in Patients with Acute Retinal Necrosis Syndrome |journal= |volume=44 |issue=6 |pages=693 |year=2000 |pmid=11094200 |doi=}}</ref> |
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==Prognosis== |
==Prognosis== |
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Revision as of 01:53, 1 July 2007
| Shingles | |
|---|---|
| Specialty | Infectious diseases, dermatology, neurology  |
Herpes zoster, colloquially known as shingles, is the reactivation (from the general area of the spinal cord) of varicella zoster virus (VZV, primary infection of which leads to chickenpox), one of the Herpesviridae group, leading to a crop of painful blisters over the area of a dermatome. In Italy and in Malta, it is sometimes referred to as "St. Anthony's fire", although that name usually refers to ergotism.[1][2] Shingles, or herpes zoster, is a neurological disease. affecting the nervous system, with or without the appearance of a rash on the skin.
Treatment is generally with antiviral drugs such as acyclovir (Zovirax), or prodrugs such as famciclovir (Famvir), or valacyclovir (Valtrex). For the antiviral drugs to be most effective, patients should begin taking them as soon as possible after the appearance of the rash, within 12 to 72 hours for maximum efficacy.[3][4]
Signs and symptoms
The earliest symptoms (constituting the prodrome) of shingles include headache, sensitivity to light, fever, and malaise, all of which may, within one to several days, be followed by itching, tingling, and extreme pain where the rash is developing. In addition, a general pain also develops in other areas of the body where affected nerves may run. (For example, pain down a leg might result in the rash elsewhere.) This pain can be characterized as stinging, tingling, aching, numbing, or throbbing, and can be pronounced with quick stabs of intensity. During this phase, herpes zoster is frequently misdiagnosed as other diseases with similar symptoms, including heart attacks and renal colic. Some patients may have these symptoms without developing the characteristic rash. This situation, known as "zoster sine herpete," can delay diagnosis and treatment.[3][5]
The initial phase is followed by development of the characteristic skin rashes of herpes zoster. The skin lesions begin as a rash, similar to hives, that follows a distribution near dermatomes, commonly occurring in a strip or belt-like pattern. The rash evolves into vesicles or small blisters filled with serous fluid. The vesicles are generally painful, and their development is often associated with the occurrence of anxiety and further flu-like symptoms, such as fever, tiredness, and generalized pain. The vesicles eventually become hemorrhagic, or filled with blood, and crust over within seven to 10 days. As the crusts fall off, patients are generally left with scarring and pigmented skin.[3]
Shingles cannot be passed from one person to another. However, the virus that causes shingles, VZV, can be spread from a person with active shingles to a person who has never had chickenpox through direct contact with the rash. The person exposed would then develop chickenpox, not shingles. The virus is not spread through sneezing, coughing or casual contact. A person with shingles can spread the disease when the rash is in the blister-phase. Once the rash has developed crusts, the person is no longer contagious. A person is not infectious before blisters appear or with post-herpetic neuralgia (pain after the rash is gone).[1][3]
Chickenpox virus can remain dormant for decades, and does so inside the ganglion near the spinal cord. As the virus is reactivated it spreads down peripheral nerve fibers and produces intense pain. The blisters therefore only affect one area of the body and do not cross the midline. They are most common on the torso, but can also appear on the face (where they are potentially hazardous to vision) or other parts of the body.[1][3]
Causes
Shingles can only arise in individuals who have had previous exposure to chicken pox (varicella zoster). Individuals develop shingles for many different reasons, most of which are thought to be a result of events which depress the immune system, such as aging, severe emotional stress, severe illness, immunosuppression or long-term use of corticosteroids.[5] However, the cellular and immunological events that lead to reactivation are poorly understood.[6] There have been recorded cases of outbreaks occurring due to unmanaged stress or other stresses to the skin such as pinching in more sensitive areas of the skin (nipples, ears, and underarms), scratching, or biting.[3]
Pathophysiology
The causative agent for herpes zoster is varicella zoster virus (VZV). Most people are infected with this virus as a child, as it causes chickenpox. The body eliminates the virus from the system, but it remains dormant in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the cranial base.
Generally, the immune system suppresses reactivation of the virus. In the elderly, whose immune response generally tends to deteriorate, as well as in those patients whose immune system is being suppressed, this process fails. (Some researchers speculate that sunburn and other, unrelated stresses that can affect the immune system may also lead to viral reactivation.) The virus starts replicating in the nerve cells, and newly formed viruses are carried down the axons to the area of skin served by that ganglion (a dermatome). Here, the virus causes local inflammation in the skin, with the formation of blisters.[1][3]
The pain characteristic of herpes zoster is thought to be due to irritation of the sensory nerve fibers in which the virus reproduces.[3]
Diagnosis
The diagnosis is visual; very few other diseases mimic herpes zoster, especially in the localization of the rash, which is otherwise quite similar in appearance and initial effect to that of poison oak or poison ivy (although it may not be accompanied by the intense itching so characteristic of those rashes).
In case of doubt, diagnostic tests can be performed. Such lab tests may be necessary because, depending on the affected sensory nerve, the pain that is experienced before the onset of the rash may be misdiagnosed as pleurisy, myocardial infarction, appendicitis, cholelithiasis, or a migraine headache. Fluid from a blister may be taken so the cells can be analyzed in a medical laboratory. While looking at the cells obtained from the blister, those infected with the herpes virus will appear very large and contain many dark nuclei. A physician can also take a viral culture of a fresh lesion, or perform a microscopic examination of the blister base called a Tzanck preparation. In a complete blood count there may be an elevated number of white blood cells, which is an indirect sign of infection. There may also be a rise in the antibody to the virus, which would also give indication of the virus’ reactivation.[3]
Treatment
Currently, there is no cure available for Herpes zoster, nor a treatment to effectively eliminate the virus from the body. However, there are some treatments that can mitigate the length of the disease and alleviate certain side effects.
Antiviral drugs
Acyclovir (an antiviral drug) inhibits replication of the viral DNA, and is used both as prophylaxis (e.g., in patients with AIDS) and as therapy for herpes zoster. Other antivirals are valacyclovir and famciclovir. During the acute phase, oral acyclovir should be given. Use of acylovir is most effective in moderating the progress of the symptoms, and in preventing post-herpetic neuralgia, if started within 24 to 72 hours of the onset of symptoms, so medical care should be obtained as soon as the condition is recognized. Immunocompromised patients may respond best to intravenous acyclovir. In patients who are at high risk for recurrences, an oral dose of acyclovir, taken twice daily, is usually effective.[7] It is also reported that the amino acid lysine inhibits the replication of herpes zoster.[8]
Other drugs
Cimetidine, a common component of over-the-counter heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances.[9][10][11] This usage is considered an off-label use of the drug. In addition, cimetidine and probenecid have been shown to reduce the renal clearance of aciclovir. [12] The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of acyclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician.
Complementary Therapies
Digestive Enzymes, are available on script and in some over the counter preparations. Before the availability of antivirals, oral pancreatic enzyme therapy in shingles was used in some countries and later subjected to clinical and scientific research. A large scale multi-centre clinical study, using an oral preparation of such enzymes, has shown promising results.[13] [14] The results of another clinical study support the concept that oral enzyme therapy is beneficial in diseases characterized in part by TGF-beta overproduction that included shingles patients. [15] TGF-B has also been found higher in instances of VZV [16] [17]
Prognosis
The rash and pain usually subside within 3 to 5 weeks. Many patients develop a painful condition called postherpetic neuralgia, which is often difficult to manage. In some patients, herpes zoster can reactivate subclinically, with pain in a dermatomal distribution without rash. This condition is known as zoster sine herpete, and may be more complicated, affecting multiple levels of the nervous system and causing multiple cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. Sometimes serious effects including partial facial paralysis (usually temporary), ear damage, or encephalitis may occur. Shingles on the upper half of the face (the first branch of the trigeminal nerve) may result in eye damage and require urgent ophthalmological assessment. Ocular complications occur in approximately one half of patients with involvement of the ophthalmic division of the trigeminal nerve. These complications include mucopurulent conjunctivitis, episcleritis, keratitis and anterior uveitis. Cranial nerve palsies of the third, fourth and sixth cranial nerves may occur, affecting extraocular motility.[7]
Since shingles is a reactivation of a virus contracted previously—often decades earlier—it cannot be induced by exposure to another person with shingles or chickenpox. Those with active blisters, however, can spread chickenpox to others who have never had that condition and who have not been vaccinated against it.[1]
Prevention
Zostavax is a vaccine developed by Merck & Co. which has proven successful in preventing half the cases of herpes zoster in a study of 38,000 people who received the vaccine.[18] The vaccine also reduced by two-thirds the number of cases of postherpetic neuralgia.[18] However, prior to the vaccine, it has long been known that adults received natural immune boosting from contact with children infected with varicella. This helped to suppress the reactivation of herpes zoster.[19] In Massachusetts, herpes zoster incidence increased 90%, from 2.77/1000 to 5.25/1000 in the period of increasing varicella vaccination 1999-2003.[20] The effectiveness of the varicella vaccine itself is dependent on this exogenous (outside) boosting mechanism. Thus, as natural cases of varicella decline, so has the effectiveness of the vaccine.[21]
The intake of micronutrients, including antioxidant vitamins, A, C, E and vitamin B, as well as fresh fruit, may reduce the risk of developing shingles. In one study, patients who consumed less than one serving of fruit a day had three times the risk as those who consumed over three servings per day. For those aged 60 or more, micronutrient and vegetable intake had a similar lowering of risk.[22] A recent study evaluated the effects of two types of behavioral intervention, Tai Chi and health education, on healthy adults, who, after 16 weeks of the intervention, were vaccinated with VARIVAX, a live attenuated Oka/Merck Varicella zoster virus vaccine.[23]
Epidemiology
Prior to implementation of the universal varicella vaccination program in the U.S., incidence of shingles increased with advancing age in association with a progressive decline in immunity to varicella-zoster virus.[18] Shingles incidence is highest in persons who are over age 55, as well as in immunocompromised patients regardless of age group.[6] The incidence rate of Herpes zoster in persons aged 65 or older is approximately 19 per 1000 individuals per year in the US. The incidence in whites of this age group is approximately 3.5 times higher than in hispanics.[24]It can also be seen in immunocompetent individuals undergoing severe emotional stress.[25]
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Herpes zoster blisters day 1. -
Herpes zoster blisters day 2. -
Herpes zoster blisters day 5. -
Herpes zoster blisters day 6, characteristic purple color.
References
- ^ a b c d e Zamula, Evelyn (2005). "Shingles:An Unwelcome Encore". United States Food and Drug Administration. Retrieved 2007-04-10.
- ^ "National Institute of Allergy and Infectious Diseases Shingles Index" (HTML). Retrieved 2007-05-17.
- ^ a b c d e f g h i Stankus, SJ (2000). "Management of Herpes Zoster (Shingles) and Postherpetic Neuralgia". American Family Physician. 61 (8): 2437–2447. PMID 10794584. Retrieved 2007-04-08.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ "Shingles (Herpes Zoster)". Centers for Disease Control. 2006. Retrieved 2007-05-30.
- ^ a b Cite error: The named reference
Mounseywas invoked but never defined (see the help page). - ^ a b Donahue, JG, Choo, PW, Manson, JE & Platt, R (1995). "The incidence of herpes zoster". Archives of Internal Medicine. 155 (15): 1605–1609. PMID 7618983.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ a b Johnson, RW & Dworkin, RH (2003). "Clinical review: Treatment of herpes zoster and postherpetic neuralgia". BMJ. 326 (7392): 748. doi:10.1136/bmj.326.7392.748.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Griffith, RS (1987). "Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis". Dermatologica. 175 (4): 183–190. PMID 3115841.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Kapinska-Mrowiecka M, &Toruwski G (1996.). "Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation". Pol Tyg Lek. 51 (23–26): 338–339. PMID 9273526.
{{cite journal}}: Check date values in:|year=(help) - ^ Hayne ST, & Mercer JB (1983). "Herpes zoster: treatment with cemetidine". Canadian Medical Association Journal. 129 (12): 1284–1285. PMID 6652595.
- ^ Notmann J, Arieli J, Hart J, Levinsky H, Halbrecht I, & Sendovsky U (1994). "In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine". Asian Pacific Journal Allergy and Immunology. 12 (1): 51–58. PMID 7872992.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ De Bony F, Tod M, Bidault R, On NT, Posner J, & Rolan P (2002). "Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir". Antimicrobial Agents and Chemotherapy. 46 (2): 458–463. PMID 11796358.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Billigmann P (1995). "[Enzyme therapy--an alternative in treatment of herpes zoster. A controlled study of 192 patients]". Fortschr. Med. (in German). 113 (4): 43–8. PMID 7713467.
- ^ Roxas M (2006). "Herpes zoster and postherpetic neuralgia: diagnosis and therapeutic considerations". Alternative medicine review : a journal of clinical therapeutic. 11 (2): 102–13. PMID 16813460.
- ^ Desser L, Holomanova D, Zavadova E, Pavelka K, Mohr T, Herbacek I (2001). "Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood". Cancer Chemother. Pharmacol. 47 Suppl: S10-5. PMID 11561866.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Kaygusuz I, Gödekmerdan A, Keleş E; et al. (2004). "The role of viruses in idiopathic peripheral facial palsy and cellular immune response". American journal of otolaryngology. 25 (6): 401–6. PMID 15547808.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - ^ Sato M, Abe T, Tamai M (2000). "Expression of the Varicella Zoster Virus Thymidine Kinase and Cytokines in Patients with Acute Retinal Necrosis Syndrome". 44 (6): 693. PMID 11094200.
{{cite journal}}: Cite journal requires|journal=(help)CS1 maint: multiple names: authors list (link) - ^ a b c Oxman, MN (2005). "A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". New England Journal of Medicine. 253 (22): 2271–2284. PMID 15930418.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Brisson M, Gay N, Edmunds W, Andrews N (2002). "Exposure to varicella boosts immunity to herpes-zoster: implications for mass vaccination against chickenpox". Vaccine. 20 (19–20): 2500–7. PMID 12057605.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Yih, WK (2005). "The incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccination coverage, 1998-2003". BMC Public Health. 5 (1): 68–68. PMID 15960856.
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External links
- National Institute of Neurological Disorders and Stroke shingles at NINDS
- NHS Choices (335)
- Emergency-Medicine.info Information about management of Shingles for physicians
- Links to pictures of Shingles (Hardin MD) University of Iowa
- After Shingles--Information about Shingles and Post-Herpetic Neuralgia