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Whilst usually a straightforward diagnosis at times the appearance can raise concern that the rash could be due to herpes simplex; however, the latter generally has a more clustered and vesicular appearance.
In uncertain cases, a scraping of a lesion can be taken and the fluid examined under the microscope. Herpes lesions will have a positive direct fluorescent antibody test. The fluid from erythema toxicum lesions will show many eosinophils. If blood samples are taken, they may show a high level of circulating eosinophils; however, this is not usually required.
Differential diagnosis may include Herpes simplex virus, Impetigo, neonatal sepsis, Listeria and Varicella (chicken pox).
Because the eruption is transient and self-limiting, no treatment is indicated.
The diagnosis is confirmed by a skin biopsy and a positive culture for acid-fast bacilli. A PPD test may also result positive.
The differential diagnoses are: acrodermatitis enteropathica, erythema infectiosum, erythema multiforme, hand-foot-and-mouth disease, Henoch–Schönlein purpura, Kawasaki disease, lichen planus, papular urticaria, papular purpuric gloves and socks syndrome, and scabies.
Diagnosis is typically obtained by an allergist or other licensed practitioner performing a cold test. During the cold test, a piece of ice is held against the forearm, typically for 3–4 minutes. A positive result is a specific looking mark of raised red hives. The hives may be the shape of the ice, or it may radiate from the contact area of the ice." However, while these techniques assist in diagnosis, they do not provide information about temperature and stimulation time thresholds at which patients will start to develop symptoms."which is essential because it can establish disease severity and monitor the effectiveness of treatment.
Solar urticaria can be difficult to diagnose, but its presence can be confirmed by the process of phototesting. There are several forms of these tests including photopatch tests, phototests, photoprovocation tests, and laboratory tests. All of these are necessary to determine the exact infliction that the patient is suffering from. Photopatch tests are patch tests conducted when it is believed that a patient is experiencing certain symptoms due to an allergy that will only occur when in contact with sunlight. After the procedure, the patient is given a low dosage of UVA radiation.
Another test known as a phototest is the most useful in identifying solar urticaria. In this test, one centimeter segments of skin are subject to varying amounts of UVA and UVB radiation in order to determine the specific dosage of the certain form of radiation that causes the urticaria to form. When testing for its less intense form (fixed solar urticaria), phototesting should be conducted only in the areas where the hives have appeared to avoid the possibility of getting false-negative results.
A third form of testing is the photoprovocation test which is used to identify disorders instigated by sun burns. The process of this test involves exposing one area of a patient's arm to certain dosage of UVB radiation and one area on the other arm to a certain dosage of UVA radiation. The amount of radiation that the patient is exposed to is equal to that "received in an hour of midday summer sun." If the procedure produces a rash, then the patient will undergo a biopsy. Finally, there are laboratory tests which generally involve procedures such as blood, urine, and fecal biochemical tests. In some situations, a skin biopsy may be performed.
The diagnosis of Gianotti–Crosti syndrome is clinical. A validated diagnostic criteria is as follows:
A patient is diagnosed as having Gianotti–Crosti syndrome if:
1. On at least one occasion or clinical encounter, he/she exhibits all the positive clinical features,
2. On all occasions or clinical encounters related to the rash, he/she does not exhibit any of the negative clinical features,
3. None of the differential diagnoses is considered to be more likely than Gianotti–Crosti syndrome on clinical judgment, and
4. If lesional biopsy is performed, the histopathological findings are consistent with Gianotti–Crosti syndrome.
The positive clinical features are:
- Monomorphous, flat-topped, pink-brown papules or papulovesicles 1-10mm in diameter.
- At least three of the following four sites involved – (1) cheeks, (2) buttocks, (3) extensor surfaces of forearms, and (4) extensor surfaces of legs.
- Being symmetrical, and
- Lasting for at least ten days.
The negative clinical features are:
- Extensive truncal lesions, and
- Scaly lesions.
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.
Erythema (redness) multiforme (EM) is usually a reaction of the skin and mucous membranes that occurs suddenly. It appears as a symmetrical rash and may include the mucous membrane lesions. This means that the body is sensitive to something that causes the skin and mucous membranes to react. The more common mild form is refer to as EM minor. It consists of a skin rash that involve no more than one mucosal surface. The sudden onset will progress rapidly as symmetrical lesions with circular color changes in some or all of the lesions. Rash will spread towards center or trunk of the body. Evenly distributed bumps on the skin become classic iris or target lesions. They have bright red borders and small white bumps in the center.
The cause of EM appears to be a highly sensitive reaction that can be triggered by a variety of causes. The causes can include bacterial, viral or chemical products, such as antibiotics – specifically penicillins or cephalosporins. This reaction is an allergic reaction and is in no way contagious.
Erythema multiforme minus is sometimes divided into papular and vesiulobullous forms.
The disease is most often diagnosed as an infant, when parents take their baby in for what appears to be bug bites. The bug bites are actually the clumps of mast cells. Doctors can confirm the presence of mast cells by rubbing the baby's skin. If hives appear, it most likely signifies the presence of urticaria pigmentosa.
Therapy for cutaneous tuberculosis is the same as for systemic tuberculosis, and usually consists of a 4-drug regimen, i.e., isoniazid, rifampin, pyrazinamide, and ethambutol or streptomycin.
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.
Autoimmune estrogen dermatitis presents as a cyclic skin disorder, that may appear eczematous, papular, bullous, or urticarial. with pruritus typically present, skin eruptions that may be chronic but which are exacerbated premenstrually or occur immediately following menses.
There is no effective treatment for this condition. It has been reported that clearance of lesions can be done with melphalan and cyclophosphamide alone or in combination with prednisone. Both isotretinoin and etretinate have also been shown to improve the conditions. All medications listed can cause adverse symptoms, with isotretinoin and etretinate particularly dangerous since they are both teratogens. Other attempted treatments include interferon-alpha, cyclosporine, PUVA photochemotherapy, electron-beam therapy, IVIg, and dermabrasion. However, the overall prognosis for the disease is poor. There are reported instances of remission of the disease when treated with a combination of Revlimid and Dexamethasone over a 24-month period.
Solar urticaria, due to its particular features, is considered to be a type of physical urticaria or light sensitivity. Physical urticaria arises from physical factors in the environment, which in the case of solar urticaria is UV radiation or light. SU may be classified based on the wavelength of the radiative energy that causes the allergic reaction; known as Harber's classification, six types have been identified in this system. Type I solar urticaria is caused by UVB (ultraviolet B) radiation, with wavelengths ranging from 290–320 nm. Type II is induced by UVA (ultraviolet A) radiation with wavelengths that can range from 320–400 nm. The wavelength range of type III and IV spans from 400 to 500 nm, while type V can be caused by UVB radiation to visible light (280–600 nm). Type VI has only been known to occur at 400 nm.
Another classification distinguishes two types. The first is a hypersensitivity caused by a reaction to photoallergens located only in people with SU; while the second is caused by photoallergens that can be found in both people with SU and people without it.
A subgroup of solar urticaria, fixed solar urticaria, has also been identified. It is a rare, less intense form of the disease with wheals (swollen areas of the skin) that affect certain, fixed areas of the body. Fixed solar urticaria is induced by a broad spectrum of radiative energy with wavelengths ranging from 300–700 nm.
The intense contact between a musical instrument and skin may exaggerate existing skin conditions or cause new skin skin conditions. Skin conditions like hyperhidrosis, lichen planus, psoriasis, eczema, and urticaria may be caused in instrumental musicians due to occupational exposure and stress. Allergic contact dermatitis and irritant contact dermatitis are the most common skin conditions seen in string musicians.
Diagnosis of aquagenic urticaria will begin with an evaluation of the patient's clinical history looking for any signs of what might be causing this severe reaction. The patient will then be put to a water treatment test where water will be applied to the upper body for 30 minutes. Water may be placed directly on the skin or a soaked paper towel may be applied. In many cases distilled water, tap water and saline will be used to check for a difference in reaction. After this is removed the skin will be checked for a reaction for the next 10–15 minutes. Because aqugenic urticaria frequently accompanies other types of physical urticaraia, the doctor may perform tests to check for these other conditions. An ice cube may be placed on the forearm for a few minutes to check for cold urticarial, exposure to a hot bath will be used to check for Cholinergis uticaria and the lesions will be inspected to determine the root cause of their appearance.
Evaluations for aquagenic urticaria consist of a clinical history and water challenge test. The standard test for aquagenic urticaria is application of a 35 °C water compress to the upper body for 30 minutes. Water of any temperature can provoke aquagenic urticaria; however, keeping the compress at a similar temperature to that of the human body (37 °C) avoids confusion with cold-induced or local heat urticaria. In addition, a forearm or hand can be immersed in water of varying temperatures. A diagnosis of aquagenic urticaria requires exclusion of other types of physical urticaria, so an exercise test and ice cube test should be performed to rule out other types of physical urticarial. aquagenic urticaria should be distinguished from aquagenic pruritus, in which brief contact with water evokes intense itching without wheals or erythema. The pathogenesis of aquagenic urticaria is not fully known; however, several mechanisms have been proposed. Interaction with water with a component in or on the stratum corneum or sebum, generating a toxic compound, has been suggested. Absorption of this substance would exert an effect of perifollicular mast cell degranulation with release of histamine.
The first-line therapy in ColdU, as recommended by EAACI/GA2 LEN/EDF/WAO guidelines, is symptomatic relief with second-generation H1- antihistamines. if standard doses are ineffective increasing up to 4-fold is recommended to control symptoms.
The second-generation H1-antihistamine, rupatadine, was found to significantly reduce the development of chronic cold urticaria symptom without an increase in adverse effects using 20 and 40 mg.
Allergy medications containing antihistamines such as diphenhydramine (Benadryl), cetirizine (Zyrtec), loratidine (Claritin), cyproheptadine (Periactin), and fexofenadine (Allegra) may be taken orally to prevent and relieve some of the hives (depending on the severity of the allergy). For those who have severe anaphylactic reactions, a prescribed medicine such as doxepin, which is taken daily, should help to prevent and/or lessen the likelihood of a reaction and thus, anaphylaxis. There are also topical antihistamine creams which are used to help relieve hives in other conditions, but there is not any documentation stating it will relieve hives induced by cold temperature.
Cold hives can result in a potentially serious, or even fatal, systemic reaction (anaphylactic shock). People with cold hives may have to carry an injectable form of epinephrine (like Epi-pen or Twinject) for use in the event of a serious reaction.
The best treatment for this allergy is avoiding exposure to cold temperature.
Studies have found that Omalizumab (Xolair) may be an effective and safe treatment to cold urticaria for patient who do not sufficiently respond to standard treatments.
Ebastine has been proposed as an approach to prevent acquired cold urticaria.
Prurigo gestationis (also called "Besnier prurigo", "Early-onset prurigo of pregnancy," "Linear IgM dermatosis of pregnancy," "Papular dermatitis of pregnancy," "Prurigo of pregnancy", and "Spangler's papular dermatitis of pregnancy") is an eruption consisting of pruritic, excoriated papules of the proximal limbs and upper trunk, most often occurring between the 20th and 34th week of gestation.
The exact etiology is unknown, but it is considered likely to be a flareup of atopic dermatitis during pregnancy.
It is sometimes considered to be a term encompassing Besnier prurigo and other conditions.
It is sometimes considered a diagnosis of exclusion.
There are no permanent cures for urticaria pigmentosa. However, treatments are possible. Most treatments for mastocytosis can be used to treat urticaria pigmentosa. Many common anti-allergy medications are useful because they reduce the mast cell's ability to react to histamine.
At least one clinical study suggested that nifedipine, a calcium channel blocker used to treat high blood pressure, may reduce mast cell degranulation in patients with urticaria pigmentosa. A 1984 study by Fairly et al. included a patient with symptomatic urticaria pigmentosa who responded to nifedipine at dose of 10 mg po tid. However, nifedipine has never been approved by the FDA for treatment of urticaria pigmentosa.
Another mast cell stabilizer Gastrocrom, a form of cromoglicic acid has also been used to reduce mast cell degranulation.
A papule (/ˈpæpjuːl/) is a circumscribed, solid elevation of skin with no visible fluid, varying in size from a pinhead to 1 cm. It can be brown, purple, pink or red in color, and can cluster into a papular rash. Papules may open when scratched and become infected and crusty. Larger non-blisterform elevated lesions may be termed nodules.
Papules may have different shapes and are sometimes associated with other features such as crusts or scales.
Granuloma annulare in HIV disease is a skin condition characterized typically by papular and generalized skin lesions.
Dermatographic urticaria (also known as dermographism, dermatographism or "skin writing") is a skin disorder and one of the most common types of urticaria affecting 2–5% of the population.
Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.
The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.
The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.
The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.
Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.
There are many skin diseases which develop papules, such as Lichen planus, a skin disease which classically forms polygonal, purple papules.