Actinic cheilitis

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Actinic cheilitis (also known as "Actinic cheilosis"[1]) is a form of cheilitis which is the counterpart of actinic keratosisof the skin and can develop into squamous cell carcinoma. In actinic cheilitis, there is thickening whitish discoloration of the lip at the border of the lip and skin. There is also a loss of the usually sharp border between the red of the lip and the normal skin, known as the vermillion border. The lip may become scaly and indurated as actinic cheilitis progresses. The lesion is usually painless, persistent, more common in older males, and more common in individuals with a light complexion with a history of chronic sun exposure.

Contents [hide]  1 Causes  2 Treatment options o 2.1 Medication o 2.2 Procedures  3 References

Causes

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Actinic cheilitis is caused by chronic and excessive exposure to ultraviolet radiation in sunlight. Additional factors may also play a role, including tobacco use, lip irritation, poor oral hygiene, and ill-fitting dentures.[2]

Treatment options

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This condition is considered premalignant because it may lead to squamous cell carcinoma in about 10% of all cases. It is not possible to predict which cases will progress into SCC, so the current consensus is that all lesions should be treated.[3]

Treatment options include 5-fluorouracil, imiquimod, scalpel vermillionectomy, chemical peel, electrosurgery, and carbon dioxide laser vaporization. These curative treatments attempt to destroy or remove the

damaged epithelium. All methods are associated with some degree of pain, edema, and a relatively low rate of recurrence.

Medication

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Topical 5-fluorouracil (5-FU, Efudex, Carac) has been shown to be an effective therapy for diffuse, but minor actinic cheilitis. 5-fluorouracil works by blocking DNAsynthesis. Cells that are rapidly growing need more DNA, so they accumulate more 5-fluorouracil, resulting in their death. Normal skin is much less affected. The treatment usually takes 2-4 weeks depending on the response. The typical response includes an inflammatory phase, followed by redness, burning, oozing, and finally erosion. Treatment is stopped when ulceration and crusting appear. There is minimal scarring. Complete clearance has been reported in about 50% of patients.[4]

Imiquimod (Aldara) is an immune response modifier that has been studied for the treatment of actinic cheilitis. It promotes an immune response in the skin leading toapoptosis (death) of the tumor cells. It causes the epidermis to be invaded by macrophages, which leads to epidermal erosion. T-cells are also activated as a result

ofimiquimod treatment. Imiquimod appears to promote an ―immune memory‖ that reduces the recurrence of lesions. There is minimal scarring. Complete clearance has been demonstrated in up to 45% of patients with actinic

keratoses. However, the dose and duration of therapy, as well as the long-term efficacy, still need to be established in the treatment of actinic cheilitis.[5]

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Both cryosurgery and electrosurgery are effective choices for small areas of actinic cheilitis. Cryosurgery is accomplished by applying liquid nitrogen in an open spraying technique. Local anesthesia is not required, but treatment of the entire lip can be quite painful. Cure rates in excess of 96% have been reported. Cryosurgeryis the treatment of choice for focal areas of actinic cheilitis. Electrosurgery is an alternate treatment, but local anesthesia is required, making it less practical than cryosurgery. With both techniques, adjacent tissue damage can delay healing and promote scar formation.[2]

More extensive or recurring areas of actinic cheilitis may be treated with either a shave vermillionectomy or a carbon dioxide laser. The shave vemillionectomy removes a portion of the vermillion ridge but leaves the

underlying muscle intact. Considerable bleeding can occur during the procedure due to the vascular nature of the lip. A linear scar may also form after treatment, but this can usually be minimized with massage and steroids. Healing time is short, and effectiveness is very high.[2]

A newer procedure uses a carbon dioxide laser to ablate the vermillion border. This treatment is relatively quick and easy to perform, but it requires a skilled operator.Anesthesia is usually required.

Secondary infection and scarring can occur with laser ablation. In most cases, the scar is minimal, and responds well to steroids. Pain can be a progressive problem during the healing phase, which can last three weeks or more. However, the carbon dioxide laser also offers a very high success rate, with very few recurrences.[2]

Chemical peeling with 50% trichloroacetic acid has also been evaluated, but results have been poor. Healing usually takes 7-10 days with very few side effects. However, limited studies show that the success rate may be lower than 30%.[2]

Herpes simplex

From Wikipedia, the free encyclopedia

"Herpes" redirects here. For the virus that causes herpes simplex, see Herpes simplex virus. For all types of herpes viruses, see Herpesviridae.

Herpes simplex

Classification and external resources

Herpes labialis of the lower lip. Note the blisters in a group marked by an arrow.

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ICD-10 A60, B00, G05.1, P35.2

ICD-9 054.0, 054.1, 054.2,054.3, 771.2

DiseasesDB 584133021

eMedicine med/1006

MeSH D006561

Herpes simplex (Greek: ἕρπης herpēs, "creeping" or "latent") is a viral disease from the herpesviridae family caused by both Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2). Infection with the herpes virus is categorized into one of several distinct disorders based on the site of infection. Oral herpes, the visible symptoms of which are colloquially called cold sores or fever blisters, is an infection of the face or mouth. Oral herpes is the most common form of infection. Genital herpes, known simply as herpes, is the second most common form of herpes. Other disorders such as herpetic whitlow, herpes gladiatorum, ocular herpes, cerebral herpes infection encephalitis, Mollaret's meningitis,neonatal herpes, and possibly Bell's palsy are all caused by herpes simplex viruses.

Herpes viruses cycle between periods of active disease—presenting as blisters containing

infectious virus particles—that last 2–21 days, followed by a remission period. Genital herpes, however, is often asymptomatic, though viral shedding may still occur. After initial infection, the viruses are transported along sensory nerves to the sensory nerve cell bodies, where they become latent and reside lifelong. Causes of recurrence are uncertain, though some potential triggers have been identified, including immunosuppressant drugs. The previously latent virus then multiplies new virus particles in the nerve cell and these are transported along the axon of each neuron to the nerve terminals in the skin, where they are released. Over time, episodes of active disease reduce in frequency and severity.

Herpes simplex is most easily transmitted by direct contact with a lesion or the body fluid of an infected individual. Transmission may also occur through skin-to-skin contact during periods of asymptomatic shedding. Barrier protection methods are the most reliable method of preventing transmission of herpes, but they merely reduce rather than eliminate risk. Oral herpes is easily diagnosed if the patient presents with visible sores or ulcers. Early stages of orofacial herpes and genital herpes are harder to diagnose; laboratory testing is usually required.

A cure for herpes has not yet been developed. Once infected, the virus remains in the body for life. Recurrent infections (outbreaks) may occur from time to time, especially in times of immune impairment such

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as HIV and cancer-related immune suppression.[1] However, after several years, outbreaks become less severe and more sporadic, and some people will become perpetually asymptomatic and will no longer experience outbreaks, though they may still be contagious to others. Treatments with antivirals can reduce viral shedding and alleviate the severity of symptomatic episodes. It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is caused by varicella zoster virus.

The differential diagnosis includes hand, foot and mouth diseasedue to similar lesions on the skin.

Contents

[hide]

 1 Classification

 2 Signs and symptoms o 2.1 Other o 2.2 Bell's palsy o 2.3 Alzheimer's disease  3 Pathophysiology  4 Diagnosis  5 Prevention o 5.1 Barrier methods o 5.2 Antivirals o 5.3 Pregnancy  6 Treatment o 6.1 Antiviral o 6.2 Topical o 6.3 Alternative medicine  7 Prognosis  8 Epidemiology  9 History

 10 Society and culture

 11 Research

 12 References

 13 External links

Classification

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Herpes simplex is divided into two types: HSV type 1 and HSV type 2. HSV1 causes primarily mouth, throat, face, eye, and central nervous system infections, whereas HSV2 causes primarily anogenital infections. However, each may cause infections in all areas.[2]

Signs and symptoms

HSV infection causes several distinct medical disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpetic whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). People with immature or suppressed immune systems, such as newborns, transplant recipients, or people with AIDS are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of bipolar disorder,[3] and Alzheimer's disease, although this is often dependent on the genetics of the infected person.

In all cases HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion.[4] As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1 infected

individuals, seroconversion after an oral infection will prevent additional HSV-1 infections such

as whitlow, genital herpes, and herpes of the eye. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted.

Many people infected with HSV-2 display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having subclinical herpes.[5]

Condition Description Illustration

Herpetic gingivostomatitis

Herpetic gingivostomatitis is often the initial presentation during the first herpes infection. It is of greater severity than herpes labialis, which is often the subsequent presentations.

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Herpes labialis Infection occurs when the virus comes into contact with oral mucosa or abraded skin.

Herpes genitalis

When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of

inflamedpapules and vesicles on the outer surface of the genitals resembling cold sores.

Herpetic whitlowand Herpes gladiatorum

Herpes whitlow is a painful infection that typically affects the fingers or thumbs. On occasion, infection occurs on the toes or on the nail cuticle. Individuals that participate in contact sports such as wrestling, rugby, and soccer sometimes acquire a condition caused by HSV-1 known as herpes

gladiatorum, scrumpox, wrestler’s herpes, or mat herpes, which presents as skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids.

Herpesviral

encephalitis andherpesviral meningitis

A herpetic infection of the brain that is thought to be caused by the retrograde transmission of virus from a peripheral site on the face following HSV-1 reactivation, along the trigeminal nerve axon, to the brain. HSV is the most common cause of viral encephalitis. When infecting the brain, the virus shows a preference for the temporal lobe.[6] HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.

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Herpes esophagitis

Symptoms may include painful swallowing (odynophagia) and difficulty swallowing (dysphagia). It is often associated with impaired immune function

(e.g. HIV/AIDS, immunosuppression in solid organ transplants).

Other

Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission of HSV (type 1 or 2) from mother to newborn. During immunodeficiency herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut.[7]Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle.[8]:369Eczema herpeticum is an infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous

areas.[8]:373Herpetic keratoconjunctivitis is a primary infection typically presents as swelling of

the conjunctiva and eyelids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea.

Bell's palsy

Although the exact cause of Bell's palsy, a type of facial paralysis, is unknown it may be related to reactivation of herpes simplex virus type 1.[9] This theory has been contested, however, since HSV is detected in large numbers of individuals having never experienced facial paralysis, and higher levels of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy compared to those without.[10] Regardless antivirals have been found to not improve outcomes.[11]

Alzheimer's disease

HSV-1 has been proposed as a possible cause of Alzheimer's disease.[12][13] In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one’s risk of developing Alzheimer’s disease. The virus interacts with the components and receptors of lipoproteins, which may lead to the development of Alzheimer's disease.[14][15]

Pathophysiology

Herpes Shedding[16]

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HSV-2 genital 15–25% of days

HSV-1 oral 6–33% of days

HSV-1 genital 5% of days

HSV-2 oral 1% of days

Herpes is contracted through direct contact with an active lesion or body fluid of an infected person.[17] Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person. Herpes simplex virus 2 is typically contracted through direct skin-to-skin contact with an infected individual but can also be contacted via exposure to infected saliva, semen, vaginal fluid or the fluid from herpetic blisters.[18] To infect a new individual, HSV travels through tiny breaks in the skin or mucous membranes in the mouth or genital areas. Even microscopic abrasions on mucous membranes are sufficient to allow viral entry.

HSV asymptomatic shedding occurs at some time in most individuals infected with herpes. It can occur more than a week before or after a symptomatic recurrence in 50% of cases.[19] Virus enters into susceptible cells via entry receptors[20] such as nectin-1, HVEM and 3-O sulfated heparan sulfate.[21] Infected people that show no visible symptoms may still shed and transmit virus through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission.[19] Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with HIV increases the frequency and duration of asymptomatic shedding.[22] There are indications that some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified; no significant differences are seen in the frequency of asymptomatic shedding when comparing persons with one to twelve annual recurrences to those with no recurrences.[19]

Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1.[citation needed] In a monogamous couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner.[23] If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection. Herpes simplex is a double stranded DNA virus.[24]

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Primary orofacial herpes is readily identified by clinical examination of persons with no previous history of lesions and contact with an individual with known HSV-1 infection. The appearance and distribution of sores in these individuals typically presents as multiple, round, superficial oral ulcers, accompanied by

acute gingivitis.[25]Adults with non-typical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergicstomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicularstage.[25]

Genital herpes can be more difficult to diagnose than oral herpes, since most HSV-2-infected persons have no classical symptoms.[25] Further confusing diagnosis, several other conditions resemble genital herpes,

including fungal infection, lichen planus, atopic dermatitis, and urethritis.[25]Laboratory testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include: culture of the virus, direct fluorescent

antibody (DFA) studies to detect virus, skin biopsy, andpolymerase chain reaction (PCR) to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.[25]

Until recently, serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice.[25] The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, the new Immunodot glycoprotein G-specific (IgG) HSV test is more than 98% specific at discriminating HSV-1 from HSV-2.[26] It is the opinion of some modern medical professionals that the new IgG test should always be clinically preferred to the old IgM test, however not all doctors appear to be informed of the availability of the newer, reliable IgG tests.[27]

Prevention

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As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.[28]On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is approximately 8–11%.[23][29]

This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is approximately 4– 5% annually.[29] Suppressive antiviral therapy reduces these risks by 50%.[30] Antivirals also help prevent the development of symptomatic HSV in infection scenarios—meaning the infected partner will be seropositive but symptom free—by about 50%. Condom use also reduces the transmission risk significantly.[31][32]

Condom use is much more effective at preventing male to female transmission than vice-versa.[31] The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk.[citation needed] These figures reflect experiences with subjects having frequently recurring genital herpes (>6 recurrences per year). Subjects with low recurrence rates and those with no clinical

manifestations were excluded from these studies.[citation needed] Previous HSV-1 infection appears to reduce the risk for acquisition of HSV-2 infection among women by a factor of 3.[33]

However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom a person will have of their own infection is the horizontal transmission to a sexual partner or the vertical

transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.[citation needed]

In October 2011, it was reported that the anti-HIV drug tenofovir, when used topically in a microbicidal vaginal gel, reduced herpes virus sexual transmission by 51%.[34]

Barrier methods

Condoms offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30% lower risk of HSV-2 acquisition compared with those that never use condoms.[35] A female condom can provide greater protection than the male condom, as it covers the labia.[36] The virus cannot pass through a synthetic condom, but a male condom's effectiveness is limited[37] because herpes ulcers may appear on areas not covered by the male condom. Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission.[38] The risk is not eliminated, however, as viral shedding capable of transmitting infection may still occur while the infected partner is asymptomatic.[39] The use of condoms or dental dams also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such asvalaciclovir, in conjunction with a condom further decreases the chances of transmission to the uninfected

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partner.[4] Topical microbicides that contain chemicals that directly inactivate the virus and block viral entry are being investigated.[4]

Antivirals

Antivirals may reduce asymptomatic shedding; it is believed asymptomatic genital HSV-2 viral shedding occurs on 20% of days per year in patients not undergoing antiviral treatment, versus 10% of days while on antiviral therapy.[19]

Pregnancy

The risk of transmission from mother to baby is highest if the mother becomes infected at around the time of delivery (30% to 60%),[40][41] since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child. In contrast, the risk falls to 3% if it is a recurrent infection,[42]and is 1–3% is the woman seropositive for both HSV-1 and HSV-2,[42][43]

and is less than 1% if there are no visible lesions.[42] Women seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1 seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g. fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect caesarean section to reduce exposure of the child to infected secretions in the birth canal.[4] The use of antiviral treatments, such as acyclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.[4]

Acyclovir is the recommended antiviral for herpes suppressive therapy during the last months of pregnancy. The use of valaciclovir and famciclovir, while potentially improving compliance have less well determined safety in pregnancy.

Treatment

There is no method to eradicate herpes virus from the body, but antiviral medications can reduce the

frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and acetaminophen can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine or tetracaine can also relieve itching and pain.[44][45][46]

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The antiviral medication acyclovir

There are several antivirals that are effective for treating herpes

including: aciclovir (acyclovir), valaciclovir (valacyclovir),famciclovir, and penciclovir. Aciclovir was the first discovered and is now available in generic.[47] Valacyclovir is also available as a generic.[48]

Evidence supports the use of aciclovir and valaciclovir in the treatment of herpes labialis[49] as well as herpes infections in people with cancer.[50] The evidence to support the use of acyclovir in primary herpetic

gingivostomatitis is less strong.[51]

Topical

A number of topical antivirals are effective for herpes labialis including acyclovir, penciclovir, and docosanol.[49][52]

Alternative medicine

Certain dietary supplements and alternative remedies are claimed to be beneficial in the treatment of herpes.[53] There is however insufficient evidence to support use of many of these compounds

including echinacea, eleuthero, L-lysine, zinc,monolaurin bee products and aloe vera.[54] While there are a number of small studies showing possible benefit from monolaurin, L-lysine, aspirin, lemon balm, topical zinc or licorice root cream in treatment, these are preliminary studies that have not been confirmed by higher

qualityrandomized controlled studies.[55]

Prognosis

Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of

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the nucleus of a nerve's cell body. HSV latency is static—no virus is produced—and is controlled by a number

of viral genes, including Latency Associated Transcript (LAT).[56]

Many HSV-infected people experience recurrence within the first year of infection.[4]Prodrome precedes development of lesions. Prodromal symptoms include tingling (paresthesia), itching, and pain where

lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the

appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop, lesions are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection.[4] Subsequent outbreaks tend to be periodic or episodic, occurring on average four to five times a year when not using antiviral therapy.

The causes of reactivation are uncertain, but several potential triggers have been documented. A recent study (2009) showed that the protein VP16 plays a key role in reactivation of the dormant virus.[57] Changes in the immune system during menstruation may play a role in HSV-1 reactivation.[58][59] Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to infection is the likely source of the historic terms cold sore andfever blister.

Other identified triggers include: local injury to the face, lips, eyes, or mouth, trauma, surgery, radiotherapy, and exposure to wind, ultraviolet light, or sunlight.[60][61][62][63][64]

The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating with large, painful lesions persisting for several weeks, while others will experience only minor itching or burning for a few days. There is some evidence that genetics plays a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes 6 genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals will experience fewer outbreaks and outbreak symptoms will often become less severe. After several years, some people will become perpetually asymptomatic and will no longer experience outbreaks, though they may still be contagious to others. Immuno-compromised individuals may experience episodes that are longer, more frequent, and more severe. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.[65]Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSV-2 infected individuals are at higher risk for

acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.[66]

Epidemiology

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Worldwide rates of either HSV-1 and/or HSV-2 are between 60-95% in adults.[2] HSV1 is more common than HSV2 with rates of both increasing as people age.[2]HSV-1 rates are between 70% to 80% in populations of low socio-economic status and 40% to 60% in populations of improved socio-economic status.[2] Prevalence of HSV-2 is those between the ages of 15 and 50 is approximately 535 million as of 2003 or 16% of the population with greater rates among women and in those in the developing world.[67] Rates of infection are determined by the presence of antibodies against either viral species.[68]

An estimated 536 million people worldwide were infected with HSV-2 in 2003, with the highest rates in sub-Saharan Africa and the lowest rates in western Europe.[69]

In the US, 57.7% of the population is infected with HSV-1[70] and 16.2% are infected with HSV-2. Among those HSV-2 seropositive, only 18.9% were aware that they were infected.[71] During 2005–2008, the prevalence of HSV-2 was 39.2% in blacks and 20.9% in women.[72]

History

Herpes has been known for at least 2,000 years. It is said that Emperor Tiberius banned kissing in Rome for a time due to so many people having cold sores. In the 16th century Romeo and Juliet, it is mentioned that there are blisters "o'er ladies' lips." In 18th century it was so common among prostitutes that it was called "a

vocational disease of women."[73] The term Herpes Simplex appeared in Richard Boulton's A System of Rational and Practical Chirurgery in 1713, where the termsHerpes miliaris and Herpes exedens also appeared. Herpes was not found to be a virus until the 1940s.[73]

Herpes antiviral therapy began in the early 1960s with the experimental use of medication that interfered with viral replication called deoxyribonucleic acid (DNA) inhibitors. The original use was against normally fatal or debilitating illness such as adult encephalitis,[74] keratitis,[75] in immunocompromised (transplant) patients,[76]or disseminated herpes zoster.[77] The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C,[78]

later marketed under the name cytosar or cytorabine. The usage expanded to include topical treatment of herpes simplex,[79] zoster, and

varicella.[80] Some trials combined different antivirals with differing results.[74] The introduction of 9-β-D-arabinofuranosyladenine, AKA ara-A or vidarabine, considerably less toxic than Ara-C, in the mid-1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U.S. Food and Drug Administration (FDA) in 1977. Other experimental antivirals of that period included: Heparin,[81] trifluorothymidine (TFT),[82] Ribivarin,[83] interferon,[84] Virazole,[85] and 5-methoxymethyl-2'-deoxyuridine (MMUdR).[86] The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA acyclovir, in the late 1970s[87] raised antiviral treatment another notch and led to vidarabine vs. acyclovir trials in the late

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of choice for herpes treatment after it was licensed by the FDA in 1998.[89] Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, something that did not occur when compared with increased dosages of vidarabine.[89] On the other side of the equation, acyclovir seems to inhibit antibody response and newborns on acyclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.[89]

Society and culture

Herpes simplex was not always stigmatised. It was merely a cold sore in an unusual place until the 1970s. As late as 1975, a study of "Psychological morbidity in a clinic for sexually transmitted disease‖ does not mention herpes simplex because at that time, there was no significant morbidity problem (i.e. mental anxiety or illness) associated with the virus.[90]

Pedro Cuatrecasas states, "during the R&D of acyclovir (Zovirax), marketing [department of Burroughs Wellcome] insisted that there were 'no markets’ for this compound. Most had hardly heard of genital herpes...‖ Thus marketing the medical condition – separating the 'normal cold sore’ from the 'stigmatized genital infection’ was to become the key to marketing the drug, a process now known as 'disease mongering’.[91][92]

Since the creation of the herpes hype, some people experience negative feelings related to the condition following diagnosis, in particular if they have acquired the genital form of the disease. Feelings can include depression, fear of rejection, feelings of isolation, fear of being found out, and self-destructive

feelings.[93] These feelings usually lessen over time. Much of the hysteria and stigma surrounding herpes stems from a media campaign beginning in the late 1970s and peaking in the early 1980s. There were multiple articles worded in fear-mongering and anxiety-provoking terminology, such as the now ubiquitous "attacks," "outbreaks," "victims," and "sufferers." At one point the term "herpetic" even entered the popular lexicon. The articles were published by Reader's Digest, U.S. News, and Time magazine, among others. A made-for-TV movie was named Intimate Agony. The peak was when Time magazine had 'Herpes: The New Scarlet Letter' on the cover in August 1982, forever stigmatizing the word in the public mind.[73]Herpes support groups have been formed in the United States and the UK, providing information about herpes and running message forums and dating websites for sufferers. People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners whom they consider casual.[94]

Research

Main article: Herpes simplex research

Researchers at the University of Florida have made a Hammerhead ribozyme that targets and cleaves the mRNA of essential genes in HSV-1. The hammerhead, which targets the mRNA of the UL20 gene, greatly reduced the level of HSV-1 ocular infection in rabbits, and reduced the viral yield in vivo.[95] The gene-targeting

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approach uses a specially designed RNA enzyme to inhibit strains of the herpes simplex virus. The enzyme disables a gene responsible for producing a protein involved in the maturation and release of viral particles in an infected cell. The technique appears to be effective in experiments with mice and rabbits, but further research is required before it can be attempted in people infected with herpes.[96]

Another possibility to eradicate the HSV-1 variant is being pursued by a team at Duke University. By figuring out how to switch all copies of the virus in the host from latency to their active stage at the same time, rather than the way the virus copies normally stagger their activity stage, leaving some dormant somewhere at all times, it is thought that conventional anti-viral drugs can kill the entire virus population completely, since they can no longer hide in the nerve cells. One class of drugs calledantagomir could serve this purpose. These are chemically engineered oligonucleotides or short segments of RNA, that can be made to mirror their target genetic material, namely herpes microRNAs. They could be engineered to attach and thus 'silence' the

microRNA, thus rendering the virus incapable of remaining latent in its host.[97] Professor Cullen believes a drug could be developed to block the microRNA whose job it is to suppress HSV-1 into latency.[98]

A chancre (/ˈʃæŋkər/ SHANG-kər)[1] is a painless ulceration (sore) most commonly formed during the primary stage ofsyphilis. This infectious lesion forms approximately 21 days after the initial exposure to Treponema pallidum, the gram-negative spirochaete bacterium yielding syphilis. Chancres transmit the sexually transmissible disease of syphilis through direct physical contact. These ulcers usually form on or around the anus, mouth, penis, and vagina. Chancres may diminish between three to six weeks without the application of medication.

In addition, chancres as well as a painless ulceration formed during the primary stage of syphilis, are associated with theAfrican trypanosomiasis sleeping sickness, surrounding the area of the tsetse fly bite.

Contents

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 1 Etymology

 2 Similarities with chancroid

 3 Differences from chancroid

 4 See also

 5 References

Etymology

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The word "chancre" (French pronunciation: ʃ ) means "little ulcer" in Old French. Related to the English "canker", they both come from the Latin cancer, meaningcrab,[2] which is a translation from the Greek word "καρκἰνος (karkínos)", also meaning crab.[3]

Similarities with chancroid

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Similarities between the conditions chancre and chancroid:

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 Both lesions are typically 1–2 cm in diameter

 Both lesions are caused by sexually transmissible organisms

 Both lesions typically appear on the genitals of infected individuals

Candidiasis

"Thrush (infection)" redirects here. For the hoof infection, see Thrush (horse).

Candidiasis

Oral candidiasis (thrush)

ICD-10 B37

ICD-9 112

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MedlinePlus 001511

eMedicine med/264emerg/76ped/312derm/67

MeSH D002177

Candidiasis or thrush is a fungal infection (mycosis) of any of the Candida species (all yeasts), of

which Candida albicans is the most common.[1][2] Also commonly referred to as a yeast infection, candidiasis is also technically known as candidosis, moniliasis, and oidiomycosis.[3]

Candidiasis encompasses infections that range from superficial, such as oral thrush and vaginitis,

to systemic and potentially life-threatening diseases. Candida infections of the latter category are also referred to as candidemia and are usually confined to severely immunocompromised persons, such

as cancer, transplant, and AIDS patients, as well as nontrauma emergency surgery patients.[4]

Superficial infections of skin and mucosal membranes by Candida causing

local inflammation and discomfort are common in many human populations.[2][5][6] While clearly attributable to the presence of the opportunistic pathogens of the genus Candida, candidiasis describes a number of different disease syndromes that often differ in their causes and outcomes.[2][5]

Contents

[hide]

 2 Signs and symptoms

 3 Causes  4 Diagnosis  5 Treatment o 5.1 Localized infection o 5.2 Blood infection  6 History

 7 Society and culture

 8 References

Classification

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Candidiasis may be divided into the following types:[3]

 Angular cheilitis (perlèche)

 Antibiotic candidiasis (iatrogenic candidiasis)

 Candidal intertrigo  Candidal paronychia

 Candidal vulvovaginitis (vaginal yeast infection)

 Candidid

 Chronic mucocutaneous candidiasis  Congenital cutaneous candidiasis  Diaper candidiasis

 Erosio interdigitalis blastomycetica  Oral candidiasis (thrush)

 Perianal candidiasis  Systemic candidiasis

Signs and symptoms

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Nail candidiasis (onychomycosis)

Symptoms of candidiasis vary depending on the area affected.[7] Most candidial infections result in minimal complications such as redness, itching and discomfort, though complications may be severe or even fatal if left untreated in certain populations. In immunocompetent persons, candidiasis is usually a very localized infection of the skin or mucosal membranes, including the oral cavity (thrush), the pharynx or esophagus,

the gastrointestinal tract, the urinary bladder, or the genitalia (vagina, penis).[1]

Candidiasis is a very common cause of vaginal irritation, or vaginitis, and can also occur on the male genitals. Inimmunocompromised patients, Candida infections can affect the esophagus with the potential of

becoming systemic, causing a much more serious condition, a fungemia called candidemia.[5][6]

Thrush is commonly seen in infants. It is not considered abnormal in infants unless it lasts longer than a few weeks.[8]

Infection of the vagina or vulva may cause severe itching, burning, soreness, irritation, and a whitish or whitish-graycottage cheese-like discharge, often with a curd-like appearance. These symptoms are also present in the more common bacterial vaginosis.[9] In a 2002 study published in the Journal of Obstetrics and Gynecology, only 33% of women who were self-treating for a yeast infection actually had a yeast infection, while most had either bacterial vaginosis or a mixed-type infection.[10] Symptoms of infection of the male genitalia include red, patchy sores near the head of the penis or on the foreskin, severe itching, or a burning sensation. Candidiasis of the penis can also have a white discharge, although uncommon.[citation needed]

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See also: Candida albicans

Candida yeasts are generally present in healthy humans, particularly on the skin, but their growth is normally limited by the human immune system, by competition of other microorganisms, such as bacteria occupying the same locations in the human body,[11] and in the case of skin, by the relative dryness of the skin,

as Candida requires moisture for growth.[12]

C. albicans was isolated from the vaginas of 19% of apparently healthy women, i.e., those who experienced few or no symptoms of infection. External use of detergents or douches or internal disturbances (hormonal or physiological) canperturb the normal vaginal flora, consisting of lactic acid bacteria, such as lactobacilli, and result in an overgrowth ofCandida cells, causing symptoms of infection, such as

local inflammation.[13] Pregnancy and the use of oral contraceptives have been reported as risk

factors.[14]Diabetes mellitus and the use of antibacterial antibiotics are also linked to an increased incidence of yeast infections.[14] Diets high in simple carbohydrates have been found to affect rates of oral

candidiases,[15] and hormone replacement therapy and infertility treatments may also be predisposing factors.[16] Wearing wet swimwear for long periods of time is also believed to be a risk factor.[2]

A weakened or undeveloped immune system or metabolic illnesses such as diabetes are significant predisposing factors of candidiasis.[17] Diseases or conditions linked to candidiasis

include HIV/AIDS, mononucleosis, cancer treatments, steroids, stress, and nutrient deficiency. Almost 15% of people with weakened immune systems develop a systemic illness caused by Candida species.[18] In extreme cases, these superficial infections of the skin or mucous membranes may enter into the bloodstream and cause systemic Candida infections.

In penile candidiasis, the causes include sexual intercourse with an infected individual, low immunity,

antibiotics, and diabetes. Male genital yeast infections are less common, and incidences of infection are only a fraction of those in women; however, yeast infection on the penis from direct contact via sexual intercourse with an infected partner is not uncommon.[19]

Candida species are frequently part of the human body's normal oral and intestinal flora. Treatment

with antibiotics can lead to eliminating the yeast's natural competitors for resources, and increase the severity of the condition.[20] Higher prevalence of colonization of C. albicans was reported in young individuals

with tonguepiercing, in comparison to unpierced matched individuals.[21] In the Western Hemisphere, about 75% of females are affected at some time in their lives.

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Agar plate culture of C. albicans

Micrograph of esophageal candidiasis showing hyphae, biopsy specimen, PAS stain

Diagnosis of a yeast infection is done either via microscopic examination or culturing.

For identification by light microscopy, a scraping or swab of the affected area is placed on a microscope slide. A single drop of 10% potassium hydroxide (KOH) solution is then added to the specimen. The KOH dissolves the skin cells, but leaves the Candida cells intact, permitting visualization of pseudohyphae and budding yeast cells typical of manyCandida species.

For the culturing method, a sterile swab is rubbed on the infected skin surface. The swab is then streaked on a culture medium. The culture is incubated at 37°C for several days, to allow development of yeast or bacterial colonies. The characteristics (such as morphology and colour) of the colonies may allow initial diagnosis of the organism causing disease symptoms.[22]

Treatment

Candidiasis is commonly treated with antimycotics; these antifungal drugs include topical clotrimazole, topical nystatin,fluconazole, and topical ketoconazole.

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A one-time dose of fluconazole is 90% effective in treating a vaginal yeast infection.[23] Local treatment may include vaginal suppositories or medicated douches. Other types of yeast infections require different

dosing. Gentian violet can be used for thrush in breastfeeding babies, but when used in large quantities, it can cause mouth and throat ulcerations, and has been linked to mouth cancer in humans and to cancer in the digestive tract of other animals.[24] C. albicans can develop resistance to fluconazole, this being more of an issue in those with HIV/AIDS who are often treated with multiple courses of fluconazole for recurrent oral infections.[25]

There is not enough evidence to determine if probiotics (either as pills or as yogurt) has an effect on the rate of occurrence of vaginal yeast infections.[26] No benefit has been found for active infections.[27]

Blood infection

In candidial infections of the blood intravenous fluconazole or an echinocandin such as caspofungin may be used.[28]Amphotericin B is another option.[28]

History

Descriptions of what sounds like oral thrush go back to the time of Hippocrates circa 460 - 370 BC.[7]

The genus Candida and species C. albicans were described by botanist Christine Marie Berkhout in her doctoral thesis at the University of Utrecht in 1923. Over the years, the classification of the genera and species has evolved. Obsolete names for this genus include Mycotorula and Torulopsis. The species has also been known in the past as Monilia albicans and Oidium albicans. The current classification is nomen conservandum, which means the name is authorized for use by the International Botanical Congress (IBC).[29]

The genus Candida includes about 150 different species; however, only a few are known to cause human infections. C. albicans is the most significant pathogenicspecies. Other species pathogenic in humans include C. tropicalis, C. glabrata, C. krusei, C. parapsilosis, C. dubliniensis, and C. lusitaniae.

Society and culture

Some alternative medicine proponents postulate a widespread occurrence of systemic candidiasis (or candida hypersensitivity syndrome, yeast allergy, fungal type dysbiosis or gastrointestinal candida overgrowth), a medically unrecognised condition.[30] The view was most widely promoted in a book published by Dr. William Crook[31] that hypothesized a variety of common symptoms such as fatigue, PMS, sexual

dysfunction, asthma, psoriasis, digestive and urinary problems, multiple sclerosis, and muscle pain could be caused by subclinical infections of C. albicans.[31] Crook suggested a variety of remedies to treat these symptoms, including dietary modification (commonly referred to as the rainbow diet—eating fresh foods and avoiding foods high in vinegar, sugar, or yeast), prescription antifungals, pau d'arco tea, echinacea tea, and colonic irrigation. With the exception of the few dietary studies in the urinary tract infection section,

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conventional medicine has not used most of these alternatives, since there is limited scientific evidence proving either their effectiveness or that subclinical systemic candidiasis is a viable diagnosis.[32][33][34][35]

In 1990, alternative health vendor Nature's Way signed an FTC consent agreement not to misrepresent in advertising any self-diagnostic test concerning yeast conditions or to make any unsubstantiated representation concerning any food or supplement's ability to control yeast conditions, with a fine of $30,000 payable to the National Institutes of Health for research in genuine candidiasis.[30]

Allergic contact dermatitis

Allergic contact dermatitis

ICD-10 L23

ICD-9 692

DiseasesDB 29435

MeSH D017449

Allergic contact dermatitis (ACD) is a form of contact dermatitis that is the manifestation of an allergic response caused by contact with a substance; the other type being irritant contact dermatitis (ICD).

Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in humans.[1]By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which these reactions occur are complex, with many levels of fine control. Their immunology centres around the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.

Contents

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 1 Pathophysiology

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 3 Symptoms  4 Treatment  5 Diagnosis  6 See also  7 References  8 Further reading

Pathophysiology

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ACD arises as a result of two essential stages: an induction phase, which primes and sensitizes the immune system for an allergic response, and an elicitation phase, in which this response is triggered (Kimble et al. 2002). As such, ACD is termed a Type IV delayed hypersensitivity reaction involving a cell-mediated allergic response. Contact allergens are essentially soluble haptens (low in molecular weight) and, as such, have the physico-chemical properties that allow them to cross the stratum corneum of the skin. They can only cause their response as part of a complete antigen, involving their association with epidermal proteins forming hapten-protein conjugates. This, in turn, requires them to be protein-reactive.

The conjugate formed is then recognized as a foreign body by the Langerhans cells (LCs) (and in some cases other Dendritic cells (DCs)), which then internalize the protein; transport it via the lymphatic system to the regional lymph nodes; and present the antigen to T-lymphocytes. This process is controlled by cytokines and chemokines - with tumor necrosis factor alpha (TNF-α) and certain members of the interleukin family (1, 13 and 18) - and their action serves either to promote or to inhibit the mobilization and migration of these LCs. (Kimble et al. 2002) As the LCs are transported to the lymph nodes, they become differentiated and transform into DCs, which are immunostimulatory in nature.

Once within the lymph glands, the differentiated DCs present the allergenic epitope associated with the allergen to T lymphocytes. These T cells then divide and differentiate, clonally multiplying so that if the allergen is experienced again by the individual, these T cells will respond more quickly and more aggressively.

White et al. have suggested that there appears to be a threshold to the mechanisms of allergic sensitisation by ACD-associated allergens (1986).[2] This is thought to be linked to the level at which the toxin induces the up-regulation of the required mandatory cytokines and chemokines. It has also been proposed that the vehicle in which the allergen reaches the skin could take some responsibility in the sensitisation of the epidermis by both assisting the percutaneous penetration and causing some form of trauma and mobilization of cytokines itself.

Allergens

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 Nickel (nickel sulfate hexahydrate) - metal frequently encountered in jewelry and clasps or buttons on clothing

 Gold (gold sodium thiosulfate) - precious metal often found in jewelry and dental materials

 Balsam of Peru (Myroxylon pereirae) - a fragrance used in perfumes and skin lotions, derived from tree resin (see also Tolu balsam). It may also be a component of artificial vanilla and/or cinnamon flavorings.

 Chromium - used in the tanning of leather. Also a component of uncured cement/mortar, facial cosmetics and some bar soaps.

 Oily coating from plants of the Toxicodendron genus: poison ivy, poison oak, and poison sumac.

 Thimerosal - a mercury compound used in local antiseptics and in vaccines

 Neomycin - a topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap and pet food. Found by itself, or in Neosporin or Triple Antibiotic

 Fragrance mix - a group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes and dental products [3]

 Formaldehyde - a preservative with multiple uses, e.g., in paper products, paints, medications, household cleaners, cosmetic products and fabric finishes. Often released into products by the use of formaldehyde releasers such as imidazolidinyl urea, diazolidinyl urea, Quaternium-15, DMDM Hydantoin and 2-bromo-2-nitropropane-1,3-diol.

 Cobalt chloride - metal found in medical products; hair dye; antiperspirant; metal-plated objects such as snaps, buttons or tools; and in cobalt blue pigment

 Bacitracin - a topical antibiotic found by itself, or as Polysporin or Triple Antibiotic

 Quaternium-15 - preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).[4]

 Colophony (Rosin) - Rosin, sap or sawdust typically from spruce or fir trees

 Topical steroid - see steroid allergy

 Photographic developers, especially those containing metol

 Topical anesthetics such as pramoxine or diphenhydramine, after prolonged use

 Methylchloroisothiazolinone/Methylisothiazolinone is a preservative used in wash-off products such as shampoos/conditioners.

Symptoms

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The symptoms of allergic contact dermatitis are very similar to the ones caused by irritant contact dermatitis, which makes the first even harder to diagnose. The first sign of allergic contact dermatitis is the presence of the rash or skin lesion at the site of exposure.[5] Depending on the type of allergen causing it, the rash can ooze, drain or crust and it can become raw, scaled or thickened. Also, it is possible that the skin lesion does not take the form of a rash but it may include papules, blisters,vesicles or even a simple red area. The main difference

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between the rash caused by allergic contact dermatitis and the one caused by irritant contact dermatitis is that the first one tends to be confined to the area where the trigger touched the skin, whereas in the second case, the rash is more likely to be more widespread on the skin.[6] Another characteristic of the allergic contact dermatitis rash is that it usually appears after a day or two after exposure to the allergen, unlike irritant contact dermatitis that appears immediately after the contact with the trigger.

Other symptoms may include itching, skin redness or inflammation, localized swelling and the area may become more tender or warmer. If left untreated, the skin may darken and become leathery and cracked.[7] Pain can also be present.

The symptoms of allergic contact may persist for as long as one month before resolving completely. Once an individual has developed a skin reaction to a certain substance it is most likely that they will have it for the rest of their life, and the symptoms will reappear when in contact with the allergen.

Treatment

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Persons who develop the rash and the other symptoms from a certain trigger are most likely to have it for the rest of their lives and detecting and avoiding the allergen is mandatory in treating the condition and resolving its symptoms.

The first step in treating the condition is applying a damp cloth shortly after the skin problem first shows to make sure that all of the irritant has been removed from the area.[8] In some cases, the best treatment is to do nothing to the area.[5]

In mild to moderate cases, patients may use skin creams containing corticosteroids to reduce the inflammation. These creams should be used carefully and according to the instructions they come with because when overused over longer periods of time they can cause serious skin conditions. Also, calamine lotion and cool oatmealbaths may relieve itching.[9] Over the counter diphenhydramine by mouth is helpful for night time itching.

Usually, severe cases are treated with systemic corticosteroids which may be tapered gradually, with various dosing schedules ranging from a total of 12 – 20 days to prevent the recurrence of the rash as well as a topical corticosteroid.[5] Tacrolimus ointment or pimecrolimus cream can also be used additionally to the corticosteroid creams or instead of these. Oral antihistamines such as diphenhydramine or hydroxyzine may also be used in more severe cases to relieve the intense itching. Topical antihistamines are not advised as there might be a second skin reactions from the lotion itself.

The other symptoms caused by allergic contact dermatitis are generally eased with wet dressings and drying lotions to stop the itching. In most cases however, medication or actual treatment is not required as long as the trigger has been identified and avoided. The discomfort caused by the symptoms may be relieved by wearing smooth-textured clothing to avoid more skin irritation or by avoiding soaps with perfumes and dyes.

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Commonly, the symptoms may resolve without treatment in 2 to 4 weeks but specific medication may hasten the healing as long as the trigger is avoided. Also, the condition might become chronic if the allergen is not detected and therefore it is not avoided.

Frequent moisturizing (and after every time you wash your hands) with organic coconut oil has found to completely cure symptoms in many sufferers.

Avoiding foods with high sources of nickel have also been found to help, particular dark chocolate, which is particularly high in nickel, as are many nuts, grains and pulses.

Diagnosis

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Diagnosing allergic contact dermatitis is primarily based on physical exam and medical history. In some cases doctors can establish an accurate diagnosis based on the symptoms that the patient experiences and on the rash's appearance. In the case of a single episode of allergic contact dermatitis, this is all that is necessary. Chronic and/or intermittent rashes which are not readily explained by history and physical exam often will benefit from further testing. A patch test (contact delayed hypersensitivity allergy test)[10] is a commonly used examination to determine the exact cause of an allergic contact dermatitis. According to the American Academy of Allergy, Asthma, and Immunology, "patch testing is the gold standard for contact allergen identification".[5]

The patch test consists in applying small quantities of potential allergens to small patches and which are then placed on the skin.[11] After two days, they are removed and if a skin reaction occurred to one of the substances applied, a raised bump will be noticeable underneath the patch. The tests are again read at 72 or 96 hours after application.

Patch testing is used for patients who have chronic, recurring contact dermatitis.[5] Other tests that may be used to diagnose contact dermatitis and rule out other potential causes of the symptoms include a skin biopsy and culture of the skin lesion.

Contact Dermatitis: Facts About Skin Rashes

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Lichen planus

Lichen planus

Lichen planus affecting the shins.

ICD-10 L43

ICD-9 697.0

DiseasesDB 7452

MedlinePlus 000867

eMedicine derm/233derm/663

MeSH D008010

Lichen planus is a chronic mucocutaneous disease that affects the skin, tongue, and oral mucosa. The disease presents itself in the form of papules,[1]lesions, or rashes. Lichen planus does not involve lichens, the fungus/algae symbionts that often grow on tree trunks; the name refers to the dry and undulating, "lichen-like"

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appearance of affected skin. It is sometimes associated with oxidative stress,[2][3] certain medications and diseases, however the underlying pathology is currently unknown.

Contents

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 2 Signs and symptoms

 3 Cause

 4 Treatment

 5 References

Classification

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Lichen planus may be divided into the following types:[4]

 Configuration

 Annular lichen planus  Linear lichen planus  Morphology of lesion

 Hypertrophic lichen planus  Atrophic lichen planus  Vesiculobullous lichen planus  Ulcerative lichen planus  Follicular lichen planus  Actinic lichen planus  Lichen planus pigmentosus

 Site of involvement

 Lichen planus of the palms and soles (Palmoplantar lichen planus)

 Mucosal lichen planus  Lichen planus of the nails

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 Inverse lichen planus

 Special forms

 Drug-induced lichen planus

 Lupus erythematosus-lichen planus overlap syndrome  Lichen planus pemphigoides

 Keratosis lichenoides chronica

 Lichenoid reaction of graft-versus-host disease  Lichenoid keratosis

 Lichenoid dermatitis

Signs and symptoms

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Lichen planus affecting the lower lip.

Micrograph of lichen planus. H&E stain.

The typical rash of lichen planus is well-described by the "6 Ps": well-defined pruritic, planar, purple, polygonal papules and plaques. The commonly affected sites are near the wrist and the ankle. The rash tends to heal with prominent blue-black or brownish discoloration that

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persists for a long time. Besides the typical lesions, many morphological varieties of the rash may occur. The presence of cutaneous lesions is not constant and may wax and wane over time. Oral lesions tend to last far longer than cutaneous lichen planus lesions.

Oral lichen planus (OLP) may present in one of three forms.

 The reticular form is the most common presentation and manifests as white lacy streaks on the mucosa (known asWickham's striae) or as smaller papules (small raised area). The lesions tend to be bilateral and are asymptomatic. The lacy streaks may also be seen on other parts of the mouth, including the gingiva (gums), the tongue, palate and lips.The reticular form is the easiest to diagnose. The bullas lesions must be

differentiated from pemphigoid, chemical burns traumatic ulcers. When they break, they appear as ulcers and need to be differentiated from squamous cell carcinoma.

 The bullous form presents as fluid-filled vesicles which project from the surface.The atrophic and erosive forms must be differentiated from lichenoid drug reactions,SLE, pemphigoids and other immunobullous disease, candidiasis, erythema multiforme.

 The erosive forms (Atrophic LP & Ulcerative LP) present with erythematous (red) areas that are ulcerated and uncomfortable. The erosion of the thin epithelium may occur in multiple areas of the mouth (more prominent on the posterior buccal mucosa), or in one area, such as the gums, where they resemble desquamative gingivitis. Wickham's striae may also be seen near these ulcerated areas. This form may undergo malignant transformation, although this is controversial. The malignant transformation rate is thought to be less than 1%, however it has been reported to be as high as 5%.[5] For any persistent oral lesion of erosive lichen planus that does not respond to topical

corticosteroids, a biopsy is recommended to rule out precancerous (premalignant) change or malignant transformation.

The microscopic appearance of lichen planus is pathognomonic for the condition

 Hyperparakeratosis with thickening of the granular cell layer

 Development of a "saw-tooth" appearance of the rete pegs

 Degeneration of the basal cell layer with Civatte or colloid body formation. These result from degenerating epithelial cells.

 Infiltration of lymphocytic inflammatorycells into the subepithelial layer of connective tissue

 epithelial connective tissue interphase weakens resulting in formation of histological cleft known as Max. Joseph's space.