Actinic Cheilitis – Pictures, Symptoms, Causes, TreatmentWritten by Dr.Mary

What is Actinic Cheilitis?This is a condition which is commonly known as “sailor’s lips” or “farmers’ lips” because this is a condition affecting the lower lips of an individual. It is really a form of actinic keratosis where rashes which are small, very often with scaly surfaces develop on the lower lips of people.

Usually this kind of problem is seen in those people who spend a lot of time outdoors in the sun and have done this for many years. It is also called accumulative sun damage for this nature.

Those with this condition frequently show other effects of skin which is damaged by the sun, for instance precancerous lesions as well as wide wrinkling. A type of cancer of the skin known as squamous cell carcinoma matures in approximately 6% to 10% of the cases of actinic cheilitis.

Actinic Cheilitis SymptomsSymptoms and signs named in a variety of sources on actinic cheilitis include the ones listed below:

Lips are dry

Lips are cracked

Lips are scaly

Lips are pale

Lips are white

Bumps that are scaly on lip

Crusty bumps on lip

Lips are red

Lips are discolored

Wrinkled lips with painless lesions

Lip puffiness

Actinic Cheilitis CausesNormally the individuals who get actinic cheilitis are those individuals who are above the age of 50 and individuals who are fair skinned. Some causes of this ailment include:

UV rays of sun

Long term use of tobacco

Smoking

Poor oral hygiene

Ill-fitting dentures

This ailment is normally due to chronic and excessive exposure to ultra-violet radiations. This is the main reason why fair skinned individuals are most susceptible to this condition, as these individuals have lesser melanin. It is also most commonly seen in older fair-skinned men.

There has been some speculation that there are other causes which may play a role in furthering the progression of this ailment. As mentioned above, the use of tobacco is one cause as well as irritation of the lips because of

chemical or physical factors such as using lip balm containing allergen. Other causes can include poor oral hygiene as well as ill-fitting dentures and prostheses seem to be responsible for further aggravating this problem.

A major risk of actinic cheilitis is that it is a precancerous condition. Actinic cheilitis has a 10% chance of turning to squamous cell carcinoma or cancer of the lip. Because it has not been identified as which kind of actinic cheilitis will develop into cancer, the standard of care is to treat all lesions properly.

Actinic Cheilitis TreatmentTreatment of actinic cheilitis includes the use of medication such as 5-fluoroucil. This medication is helpful for minor actinic cheilitis. This medication works by blocking DNA synthesis. Treatment with this medication normally takes up to a month to yield any type of results which are visible. Initially with treatment there will be inflammation with redness, erosion and burning of lesions. Approximately 50% of individuals do respond well to this management and are reported to have gone into total remission.

Another medication which is reported to have good results is imioquimod cream. This medication is an immune response modifier and therefore promotes an immune response in the skin that leads to the erosion as well as the death of the epidermal growth and remission of the rash on lips. It also aids in preventing any recurrence of the lesions.

However, there are many cases that do not adequately respond to medications. In these cases, other options include procedures such as:

Cryosurgery

Electrosurgery

These treatments are the standard of care for small lesions of actinic cheilitis.

Cryosurgery is the application of liquid nitrogen as an open spray. Local anesthesia is not necessary but if there is need of treating the entire lip, then this process could end up being very painful. This treatment is reported to have a very high rate of success and therefore is the treatment of choice for focal areas of actinic cheilitis.Electrosurgery also referred to as electrodesiccation is a treatment alternative that needs local anesthesia. Both of these techniques lead to tissue which is adjacent to be damaged and can therefore delay healing as well as leading to the formation of scars.There is also a technique of facial sanding known as dermabrasion.

There is a fairly new procedure for dealing with this ailment that involves using carbon dioxide laser to ablate or shave the vermillion border. This procedure is known as vermilionectory. But this process can also run the risk of causing secondary infections and scarring. Another option is chemical peeling using 50% trichloroacetic acid except results have not been very satisfactory,

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 (Ancient Greek: ἕρπης – herpes, "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 (keratitis),

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 life-long. 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

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. Vaccines are in clinical trials but have not demonstrated effectiveness. 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 disease due to

similar lesions on the skin.

Classification

Herpes simplex is divided into two types: HSV type 1 and HSV type 2.[2] HSV1 causes primarily mouth, throat, face, eye, and central nervous system infections, whereas HSV2 causes primarily anogenital infections.[2] 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). Patients with immature or suppressed immune systems, such as newborns, transplant recipients, or AIDS patients 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,[4] 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.[5] 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 keratitis. 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.[6]

Diagnosis

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.[26] 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 allergic stomatitis. 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 vesicular stage.[26]

Genital herpes can be more difficult to diagnose than oral herpes, since most HSV-2-infected persons have no classical symptoms.[26] Further confusing diagnosis, several other conditions resemble genital herpes, including fungal infection, lichen planus, atopic dermatitis, and urethritis.[26] 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, and polymerase 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.[26]

Until recently, serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice.[26] 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.[27] 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.[28]

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 andacetaminophen can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine or tetracaine can also relieve itching and pain.[

Chancre

From Wikipedia, the free encyclopedia

Chancre on the underside of the penis

A chancre ( / ̍ ʃ æ ŋ k ər / SHANG -kər)[1] is a painless ulceration (sore) most commonly formed during the primary

stage of syphilis. This infectious lesionforms 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 the African trypanosomiasissleeping sickness, surrounding the area of the tsetse fly bite.

Candidiasis

From Wikipedia, the free encyclopedia

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

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 immunocompromisedpersons, 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]

Classification

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

Skin candidiasis

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 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, theurinary 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.

In immunocompromised patients, Candidainfections can affect the esophagus with the potential of

becoming systemic, causing a much more serious condition, a fungemia calledcandidemia.[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-

gray cottage 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]

Causes

See also: Candida albicans

Candida yeasts are commonly present in humans, and their growth is normally limited by the human immune

system and by other microorganisms, such as bacteria occupying the same locations in the human body.[11]

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) can perturb the normal vaginal flora, consisting of lactic acid bacteria, such as lactobacilli, and result

in an overgrowth of Candida cells, causing symptoms of infection, such as local inflammation.[12] Pregnancy and the

use of oral contraceptives have been reported as risk factors.[13] Diabetes mellitus and the use of

antibacterial antibiotics are also linked to an increased incidence of yeast infections.[13] Diets high in

simple carbohydrates have been found to affect rates of oral candidiases,[14] and hormone replacement

therapy and infertility treatments may also be predisposing factors.[15] 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.[16] 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.[17] 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.[18]

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.[citation needed] Higher prevalence of colonization of C. albicans was reported in young individuals

with tongue piercing, in comparison to unpierced matched individuals.[19] In the Western Hemisphere, about 75%

of females are affected at some time in their lives.

Diagnosis

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 many Candida 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.[20]

Treatment

In clinical settings, candidiasis is commonly treated with antimycotics; the antifungal drugs commonly used to treat

candidiasis are topical clotrimazole, topical nystatin, fluconazole, and topical ketoconazole.

For example, a one-time dose of fluconazole (150-mg tablet taken orally) has been reported as being 90% effective

in treating a vaginal yeast infection.[21] This dose is only effective for vaginal yeast infections, and other types of

yeast infections may require different dosing. In severe infections,amphotericin B, caspofungin,

or voriconazole may be used. Local treatment may include vaginal suppositories or medicated douches. 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.[22]

Chlorhexidine gluconate oral rinse is not recommended to treat candidiasis,[23] but is effective as prophylaxis;[24] chlorine dioxide rinse was found to have similar in vitro effectiveness against Candida.[25]

C. albicans can develop resistance to antimycotic drugs.[26] Recurring infections may be treatable with other

antifungal drugs, but resistance to these alternative agents may also develop.

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).[27]

The genus Candida includes about 150 different species; however, only a few are known to cause human

infections. C. albicans is the most significant pathogenic species. 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, or gastrointestinal candida overgrowth), a medically unrecognised

condition.[28] The view was most widely promoted in a book published by Dr. William Crook[29] 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.[29] Crook

suggested a variety of remedies to treat these symptoms, including dietary modification, prescription antifungals,

and colonic irrigation. With the exception of the few dietary studies in the urinary tract infectionsection,

conventional medicine has not used most of these alternatives, since limited scientific evidence proves either their

effectiveness or subclinical systemic candidiasis is a viable diagnosis.[30][31][32][33]

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.[28]

Contact dermatitis

Contact dermatitis is a term for a skin reaction (dermatitis) resulting from exposure to allergens (allergic contact

dermatitis) or irritants (irritant contact dermatitis). Phototoxic dermatitis occurs when the allergen or irritant is

activated by sunlight.

[edit]Symptoms

Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance. Only the

superficial regions of the skin are affected in contact dermatitis.Inflammation of the affected tissue is present in

the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis).[1] Unlike contact urticaria, in which a rash appears within minutes of exposure and fades away within minutes to

hours, contact dermatitis takes days to fade away. Even then, contact dermatitis fades only if the skin no longer

comes in contact with the allergen or irritant.[2] Contact dermatitis results in large, burning, and itchy rashes, and

these can take anywhere from several days to weeks to heal. Chronic contact dermatitis can develop when the

removal of the offending agent no longer provides expected relief.

[edit]Causes

In the Americas, the most common causes of allergic contact dermatitis are plants of

the Toxicodendron genus: poison ivy, poison oak, and poison sumac. Specific plant species that can induce such

contact dermatitis include Western Poison Oak, a widespread plant in the western USA.[3]

The alkyl resorcinols in Grevillea banksii and Grevillea 'Robyn Gordon' are responsible for contact dermatitis.[4] Bilobol, another alkyl resorcinol found in Gingko biloba fruits is a strong skinirritant.[5]

Other common causes of irritant contact dermatitis are harsh (highly alkaline) soaps, detergents, and cleaning

products.[6]

[edit]Types

There are three types of contact dermatitis: irritant contact dermatitis, allergic contact dermatitis, and

photocontact dermatitis. Photocontact dermatitis is divided into two categories that is, phototoxic and

photoallergic.

[edit]Irritant contact dermatitis

Main article: Irritant contact dermatitis

Irritant contact dermatitis can be divided into forms caused by chemical irritants and those caused by physical

irritants. Common chemical irritants implicated include solvents (alcohol, xylene,turpentine,

esters, acetone, ketones, and others); metalworking fluids (neat oils, water-based metalworking fluids with

surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl

sulfate); alkalies (drain cleaners, strong soap with lye residues). Physical irritant contact dermatitis may most

commonly be caused by low humidity from air conditioning.[7] Also, many plants directly irritate the skin.

[edit]Allergic contact dermatitis

Main article: Allergic contact dermatitis

Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in

humans.[8] By its allergic nature, this form of contact dermatitis is a hypersensitivereaction 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. Allergens include nickel, gold, balsam of Peru (Myroxylon pereirae), chromium and the oily coating

from plants of theToxicodendron genus: poison ivy, poison oak, and poison sumac.

[edit]Photocontact dermatitis

Sometimes termed "photoaggravated",[9] and divided into two categories, phototoxic and photoallergic, PCD is the

eczematous condition which is triggered by an interaction between an otherwise unharmful or less harmful

substance on the skin and ultraviolet light (320-400 nm UVA) (ESCD 2006), therefore manifesting itself only in

regions where the sufferer has been exposed to such rays. Without the presence of these rays, the photosensitiser

is not harmful. For this reason, this form of contact dermatitis is usually associated only with areas of skin which

are left uncovered by clothing, and it can be soundly defeated by avoiding exposure to sunlight.[10] The mechanism

of action varies from toxin to toxin, but is usually due to the production of a photoproduct. Toxins which are

associated with PCD include the psoralens. Psoralens are in fact used therapeutically for the treatment of psoriasis,

eczema and vitiligo.

Photocontact dermatitis is another condition where the distinction between forms of contact dermatitis is not

clear cut. Immunological mechanisms can also play a part, causing a response similar to ACD.

[edit]Symptoms

Allergic dermatitis is usually confined to the area where the trigger actually touched the skin, whereas irritant

dermatitis may be more widespread on the skin. Symptoms of both forms include the following:

Red rash. This is the usual reaction. The rash appears immediately in irritant contact dermatitis; in allergic

contact dermatitis, the rash sometimes does not appear until 24–72 hours after exposure to the allergen.

Blisters or wheals. Blisters, wheals (welts), and urticaria (hives) often form in a pattern where skin was directly

exposed to the allergen or irritant.

Itchy, burning skin. Irritant contact dermatitis tends to be more painful than itchy, while allergic contact

dermatitis often itches.

While either form of contact dermatitis can affect any part of the body, irritant contact dermatitis often affects the

hands, which have been exposed by resting in or dipping into a container (sink, pail, tub, swimming pools with high

chlorine) containing the irritant.

[edit]Treatment

[edit]Self-care at home

Immediately after exposure to a known allergen or irritant, wash with soap and cool water to remove or

inactivate most of the offending substance.

Weak acid solutions [lemon juice, vinegar] can be used to counteract the effects of dermatitis contracted by

exposure to basic irritants.

If blistering develops, cold moist compresses applied for 30 minutes 3 times a day can offer relief.

Calamine lotion and cool colloidal oatmeal baths may relieve itching.

Oral antihistamines such as diphenhydramine (Benadryl, Ben-Allergin) can also relieve itching.

For mild cases that cover a relatively small area, hydrocortisone cream in nonprescription strength may be

sufficient.

Avoid scratching, as this can cause secondary infections.

A barrier cream such as those containing zinc oxide (e.g. Desitin, etc.) may help to protect the skin and retain

moisture.

[edit]Medical care

If the rash does not improve or continues to spread after 2-3 of days of self-care, or if the itching and/or pain is

severe, the patient should contact a dermatologist or other physician or physician assistant. Medical treatment

usually consists of lotions, creams, or oral medications.

Corticosteroids. A corticosteroid medication similar to hydrocortisone may be prescribed to combat

inflammation in a localized area. This medication may be applied to the skin as a cream or ointment. If the

reaction covers a relatively large portion of the skin or is severe, a corticosteroid in pill or injection form may

be prescribed.

Antihistamines. Prescription antihistamines may be given if nonprescription strengths are inadequate.

[edit]Prevention

Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to

identify the responsible agent and avoid it. This can be accomplished by having patch tests, a method commonly

known as allergy testing. The patient must know where the irritant or allergen is found to be able to avoid it. It is

important to also note that chemicals sometimes have several different names.[11]

In an industrial setting the employer has a duty of care to the individual worker to provide the correct level of

safety equipment to mitigate the exposure to harmful irritants. This can take the form of protective clothing,

gloves or barrier cream depending on the working environment.