In the United States, only about 4% of patients with photosensitive disorders are reported to have been diagnosed with solar urticaria. Internationally, the number is slightly larger at 5.3%. Solar urticaria may occur in all races but studies monitoring 135 African Americans and 110 Caucasians with photodermatoses found that 2.2% of the African Americans had SU and 8% of the Caucasians had the disease showing that Caucasians have a better chance of getting the disease. Globably 3.1 per 100,000 people are affected and females are more likely to be affected than males. The age ranges anywhere from 5–70 years old, but the average age is 35 and cases have been reported with children that are still in infancy. Solar urticaria accounts for less than one percent of the many documented urticaria cases. To put that into a better perspective, since its first documented case in Japan in 1916, over one hundred other instances of the disease have been reported.

Solar urticaria is an immunoglobulin E-mediated hypersensitivity that can be introduced through primary or secondary factors, or induced by exogenous photosensitization. Primary SU is believed to be a type I hypersensitivity (a mild to severe reaction to an antigen including anaphylaxis) in which an antigen, or substance provoking an immune response, is "induced by UV or visible radiation." Secondary SU can occur when a person comes into contact with chemicals such as tar, pitch, and dyes. People who use drugs such as benoxaprofen or patients with erythropoietic protoporphyria may also contract this secondary form. These items that cause this photosensitivity are exogenous photosensitizers because they are outside of the body and cause it to have a greater sensitivity to light.

Also, there have been a few unorthodox (unusual) causes of solar urticaria. For those susceptible to visible light, white T-shirts may increase the chances of experiencing an outbreak. In one case, doctors found that the white T-shirt absorbed UVA radiation from the sun and transformed it into visible light which caused the reaction. Another patient was being treated with the antibiotic tetracycline for a separate dermatological disorder and broke out in hives when exposed to the sun, the first case to implicate tetracycline as a solar urticaria inducing agent.

It is not yet known what specific agent in the body brings about the allergic reaction to the radiation. When patients with SU were injected with an irradiated autologous serum, many developed urticaria within the area of injection. When people who did not have SU were injected, they did not demonstrate similar symptoms. This indicates that the reaction is only a characteristic of the patients with solar urticaria and that it is not phototoxic. It is possible that this photoallergen is located on the binding sites of IgE that are found on the surface of mast cells. The photoallergen is believed to begin its configuration through the absorption of radiation by a chromophore. The molecule, because of the radiation, is transformed resulting in the formation of a new photoallergen.

The more poignant part of this disorder is the lack of desensitization for water and aqua intile injection as allergen even on repeated exposure. Avoidance of allergen as a general principle in any allergic disorder necessitates the evasion of water exposure. Topical application of antihistamines like 1% diphenhydramine before water exposure is reported to reduce the hives. Oil in water emulsion creams, petrolatum as barrier agents for water can be used prior to shower or bath with good control of symptoms. Therapeutic effectiveness of various classes of drugs differs from case to case.

Irritant contact dermatitis (ICD) 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); and alkalis (drain cleaners, strong soap with lye residues).

Physical irritant contact dermatitis may most commonly be caused by low humidity from air conditioning. Also, many plants directly irritate the skin.

Symptoms are thought to be the result of histamine being released by mast cells on the surface of the skin. Due to the lack of antigens, histamine causes the skin to swell in affected areas. If the membrane that surrounds the mast cells is too weak it will easily and rapidly break down under physical pressure, which will therefore cause an allergic-like reaction.

Symptoms can be caused or induced by

- stress

- tight or abrasive clothing

- watches

- glasses

- heat

- cold

- anything placing pressure on exposed skin

- infection

The underlying cause of dermatographism is not known, and can last for many years without relief. The condition may subside and be effectively cured; however, it is often a lifelong ailment. It is not a life-threatening disease and is not contagious.

Dermographism may occur in Mastocytosis (systemic mast cell proliferation).

Chronic idiopathic hives has been anecdotally linked to stress since the 1940s. A large body of evidence demonstrates an association between this condition and both poor emotional well-being and reduced health-related quality of life. A link between stress and this condition has also been shown. A recent study has demonstrated an association between stressful life events (e.g. bereavement, divorce, etc.) and chronic idiopathic urticaria and also an association between post-traumatic stress and chronic idiopathic hives.

The most common food allergies in adults are shellfish and nuts. The most common food allergies in children are shellfish, nuts, eggs, wheat, and soy. One study showed Balsam of Peru, which is in many processed foods, to be the most common cause of immediate contact urticaria. A less common cause is exposure to certain bacteria, such as "Streptococcus" species or possibly "Helicobacter pylori".

The cause of physical urticaria is unknown but it has been suggested to be an autoimmune disease. Suggesting that antibodies, which are produced by the immune system to protect humans from foreign microbes, are binding to body tissue; damaging body tissue.

In some cases physical urticaria can be a symptom of an underlying health issue such as:

- thyroid disease

- hepatitis

- infection

- cancer.

Or can also be due to:

- food allergies

- atopy

Allergic contact dermatitis (ACD) is accepted to be the most prevalent form of immunotoxicity found in humans, and is a common occupational and environmental health problem. By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which this reaction occurs are complex, with many levels of fine control. Their immunology centres on 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 the "Toxicodendron" genus, such as poison ivy, poison oak, and poison sumac.

Aquagenic urticaria, once known as a rare physical urticaria, is reclassified as separate subtype of urticaria. It was first reported by Walter B Shelley et al. in 1964. Pruritic hives on contact with water mostly presenting for the first time during puberty in females of reproductive age is seen in aquagenic urticaria. Males are less often affected. Even if majority cases are sporadic in nature, familial cases are also recorded. Water in all forms such as tap or sea water, swimming pool, sweat, tears, saliva can induce the lesions.

Several factors can worsen the symptoms of urticaria pigmentosa:

- Emotional stress

- Physical stimuli such as heat, friction, and excessive exercise

- Bacterial toxins

- Venom

- Eye drops containing dextran

- NSAIDs

- Alcohol

- Morphine

The classification of NSAIDs can be disputed. Aspirin, for example, causes the mast cells to degranulate, releasing histamines and causing symptoms to flare. However, "daily" intake of 81 mg aspirin may keep the mast cells degranulated. Thus, while symptoms may be worsened at first, they can get better as the mast cells are unable to recharge with histamine.

Familial cold urticaria (also properly known as familial cold autoinflammatory syndrome, FCAS) is an autosomal dominant condition characterized by rash, conjunctivitis, fever/chills and arthralgias elicited by exposure to cold - sometimes temperatures below 22 °C (72 °F).

It has been mapped to CIAS1 and is a slightly milder member of the disease family including Muckle–Wells syndrome and NOMID. It is rare and is estimated as having a prevalence of 1 per million people and mainly affects Americans and Europeans.

FCAS is one of the cryopyrin-associated periodic syndromes (CAPS) caused by mutations in the CIAS1/NALP3 (aka NLRP3) gene at location 1q44. The disease was described in The Lancet Volume 364 by Hoffman H.M. et al.

The effect of FCAS on the quality of life of patients is far reaching. A survey of patients in the United States in 2008 found, "To cope with their underlying disease and to try to avoid symptomatic, painful, flares patients reported limiting their work, school, family, and social activities. Seventy-eight percent of survey participants described an impact of the disease on their work, including absenteeism and impaired job advancement; frequently, they quit their job as a consequence of their disease".

Treatment using anakinra (Kineret) has been shown effective for FCAS, although this does mean daily injections of the immunosuppressant into an area such as the lower abdomen. The monoclonal antibody canakinumab (Ilaris) is also used.

Reflex cold urticaria is a cutaneous condition in which generalized cooling of the body induces widespread ing.

Dermographism can be treated by substances (i.e. an antihistamine) which prevent histamine from causing the reaction. These may need to be given as a combination of H antagonists, or possibly with an H-receptor antagonist such as cimetidine.

OTC Vitamin C, 1000 mg daily, increases histamine degradation and removal.

Not taking hot baths or showers may help if it is generalized (all over) and possibly for localized cases (in a specific area). If taking hot showers helps, it may be a condition called shower eczema. If it affects mainly the head, it may be psoriasis. In rare cases, allergy tests may uncover substances the patient is allergic to.

While cromoglycate, which prevents histamine from being released from mast cells, is used topically in rhinitis and asthma, it is not effective orally for treating chronic urticaria.

The majority of urticaria pigmentosa cases are caused by a point mutation at amino acid 816 of the proto-oncogene c-kit. c-kit is a transmembrane protein which, when bound to Mast Cell Growth Factor (MCGF), signals the cell to divide. Mutations in position 816 of c-kit can result in a constant division signal being sent to the mast cells, resulting in abnormal proliferation. Different mutations have been linked to different onset times of the disease.

For example, the Asp816Phe and Asp816Val mutations (the aspartate normally at position 816 in the c-kit protein has been replaced with phenylalanine or valine respectively) have been associated with early manifestation of the disease (mean age of onset: 1.3 and 5.9 months respectively).

The c-kit gene is encoded on the q12 locus of chromosome 4.

Antihistamine agents are the typically prescribed drug for the treatment of physical urticaria. They block the effect of histamine, a compound produced by the body which forms a part of the local immune response consequently causing inflammation. Some research has suggested that the use antihistamines and antagonist in synergy are better for the treatment of physical urticarias.

The cascade of events that link the autoantibody-antigen reaction with the production and release of histamine is not well characterized. Therefore, the focus of treatment for physical urticaria has been on characterizing the effectiveness of antihistamines rather than analysis of receptor binding or the pathomechanisms.

Occupational skin diseases are ranked among the top five occupational diseases in many countries.

Contact Dermatitis due to irritation is inflammation of the skin which results from a contact with an irritant. It has been observed that this type of dermatitis does not require prior sensitization of the immune system. There have been studies to support that past or present atopic dermatitis is a risk factor for this type of dermatitis. Common irritants include detergents, acids, alkalies, oils, organic solvents and reducing agents.

The acute form of this dermatitis develops on exposure of the skin to a strong irritant or caustic chemical. This exposure can occur as a result of accident at a workplace . The irritant reaction starts to increase in its intensity within minutes to hours of exposure to the irritant and reaches its peak quickly. After the reaction has reached its peak level, it starts to heal. This process is known as decrescendo phenomenon. The most frequent potent irritants leading to this type of dermatitis are acids and alkaline solutions. The symptoms include redness and swelling of the skin along with the formation of blisters.

The chronic form occurs as a result of repeated exposure of the skin to weak irritants over long periods of time.

Clinical manifestations of the contact dermatitis are also modified by external factors such as environmental factors (mechanical pressure, temperature, and humidity) and predisposing characteristics of the individual (age, sex, ethnic origin, preexisting skin disease, atopic skin diathesis, and anatomic region exposed.

Another occupational skin disease is glove-related hand urticaria, believed to be caused by repeated wearing and removal of the gloves. It has been reported as an occupational problem among the health care workers. The reaction is caused by the latex or the nitrile present in the gloves.

Urticarial dermatoses are distinct from urticaria, which examples being drug-induced urticaria, eosinophilic cellulitis and bullous pemphigoid. It is important to distinguish urticaria from urticarial dermatoses. The individual wheals of urticaria are ‘here today and gone tomorrow’ (i.e. they last less than 24 hours), whereas with urticarial dermatoses, the individual lesions last for days or longer.

Prevention measures include avoidance of the irritant through its removal from the workplace or through technical shielding by the use of potent irritants in closed systems or automation, irritant replacement or removal and personal protection of the workers.

A sweat allergy is the exacerbation of atopic dermatitis associated with an elevated body temperature and resulting increases in the production of sweat. It appears as small reddish wheals that become visible in response to increased temperature and resulting production of sweat. It can effect all ages. Sweating can trigger intense itching or cholinergic urticaria. The protein MGL_1304 secreted by mycobiota present on the skin such as "Malassezia globosa" acts as a histamine or antigen. People can be desensitized using using their own samples of sweat that have been purified that contains small amounts of the allergen. The allergy is not due to the sweat itself but instead to an allergy-producing protein secreted by baceria found on the skin.

Cholinergic urticaria (CU) is one of the physical urticaria which is provoked during sweating events such as exercise, bathing, staying in a heated environment, or emotional stress. The hives produced are typically smaller than classic hives and are generally shorter-lasting.

Multiple subtypes have been elucidated, each of which require distinct treatment.

Tannic-acid has been found to suppress the allergic response along with showering.

Rosin, the material commonly used to wax string instruments is known to cause allergic contact dermatitis in musicians. Nickel, a metal found in musical instruments causes allergic contact dermatitis on the fingers and hands of string instrumentalists and in the lip and neck of wind instrumentalists. Wind instrumentalists with lip and neck infection should switch to gold or plastic mouthpieces if allergic dermatitis occurs. (R)-4-methoxydalbergione present in rosewood may cause allergic contact dermatitis in violinists. Cane reed (causing chelitis in saxophone players), propolis (a wax used to close structural gaps in musical instruments), paraphenylenediamine (used to polish musical instruments) and potassium dichromate (tanning agent to the skin of the harp) also cause allergic contact dermatitis in musicians.

Unknown or unclassified at this time. This represents those who do not fall under any of the above categories.

Frequent, chronic contact of instruments to skin may make it callous by the thickening of stratum corneum. Use of 'thumb position' in cellists may cause callosity of left thumb. Garrod's pads are seen on the dorsal left second and third fingers over the proximal interphalangeal joints in violinists. Drummer's digit is the callosity seen on the lateral phalynx of the left finger. Callosities need treatment only when they are excessive or symptomatic.

The wheals, hypohidrosis, and pain seems to result from the low expression levels of acetylcholinesterase (AchE) and cholinergic receptor, muscarinic 3 (CHRM3) in the eccrine gland epithelial cells.

Elevated expression levels of CCL2/MCP-1, CCL5/RANTES and CCL17/TARC which result in chemoattracted CD4+ and CD8+ T cell populations to the surrounding area may be responsible for exerting a downmodulatory effect on the AchE and CHRM3 expressions.

Corticosteroid inhibits the expressions of CCL2/MCP-1, CCL5/RANTES and CCL17/TARC. This further support the notion that CCL2/MCP-1, CCL5/RANTES and CCL17/TARC play a crucial role.

It was noted that although antihistamines and anti-inflammatory drugs such as, colchicine, sulphasalazine, dapsone, and topical steroid are advocated for in the treatment of DPU, most if not all are unsatisfactory in relieving symptoms. Even a second generation antihistamine, ketotifen, was unable to efficiently and satisfactorily relieve symptoms of DPU