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Schamberg's disease is caused by leaky blood vessels near the surface of the skin, capillaries, which allow red blood cells to slip through into the skin. The red blood cells in the skin then fall apart and release their iron, which is released from hemoglobin. The iron causes a rust color and this accounts for the orange tint of the rash that can be seen on the skin. The underlying cause of the leaky blood vessels is not known, but researchers are suggesting that there could be some potential triggers. Some possible triggers include viral infection, a hypersensitivity to some agent, and interaction of some medications, such as thiamine and aspirin. Even though there is no correlation with genetics, there have been a few cases where few people in a family had this condition.
Although the cause of capillary inflammation is unknown, certain preventive measures can be taken. Doctors may prescribe medications that enhance the circulation of blood, which can keep blood vessels strong and healthy. Daily intake of vitamin C has proven to be a natural home remedy that can prevent the onsite of any disease or infection. Doctors always recommend that their patients monitor what they eat because their diet could be a possible factor that contributes to this condition. A healthy body that receives nutritious meals is more likely to have a healthy life that does not revolve around a lot of health problems.
There is no cure for Schamberg's disease; however, the itching can be controlled by a cortisone cream, and Colchicine treatment has been successfully used to prevent recurrence of the symptoms. This condition is not life-threatening or a major health concern. The only problem that patients will encounter is the itching and discoloration of the skin. It is recommended that patients take a vitamin C supplement to promote collagen production, which will help make the skin look and feel healthier. To prevent further irritation of the lesions, patients should avoid food with artificial colors and preservatives. Some people can be allergic to preservatives, which can cause the body to initiate an allergic reaction by further irritating those lesions. Several research studies have indicated that Schamberg's disease can be controlled and the number of lesions can be reduced with use a drug called aminaphtone. This drug helps improve capillary fragility and it prevents and controls the purpuric lesions.
A patient with Schamberg's disease can live a normal and healthy life. Since there is no proven cure for this condition, the patient will have to endure the lesions on his or her skin. With appropriate treatments, the condition may get better. Although the skin lesions are not life-threatening, it may cause a cosmetic concern for some individuals. Skin lesions may cause psychological discomfort, where patients may require reassurance to help with stress and anxiety. There are a few rare cases of T-cell lymphoma that has developed from Schamberg's disease.This is not a cause for concern, since the risk factors associated with Schamberg's disease are relatively low.
Solar purpura (also known as "Actinic purpura," and "Senile purpura") is a skin condition characterized by large, sharply outlined, 1- to 5-cm, dark purplish-red ecchymoses appearing on the dorsa of the forearms and less often the hands.
The condition is most common in elderly people of European descent. It is caused by sun-induced damage to the connective tissue of the skin.
No treatment is necessary. The lesions typically fade over a period of up to 3 weeks.
Doucas and Kapetanakis pigmented purpura is a skin condition characterized by scaly and eczematous patches, which also have petechiae and hemosiderin staining.
It is also known as "eczematoid purpura" or "eczematoid-like purpura".
It was characterized in 1953.
Pigmented purpuric dermatosis (also known as "progressive pigmentary dermatosis," "purpura pigmentosa chronica," "pigmentary purpuric eruptions," or "progressive pigmenting purpura" or "Schamberg's disease") refers to one of the three major classes of skin conditions characterized by purpuric skin eruptions.
Pigmented purpuric dermatosis are distinguished from other purpura by size (0.3–1 cm) and are most often seen in the lower extremities. Pigmentary purpuric eruptions may present with one of several clinical patterns. There may be overlapping characteristics among pigmented purpuric dermatosis and between their signs and those of other purpuric eruptions. Examples of the pigmented purpuric dermatosis group include:
Although vascular damage may be present, it is insufficient for these conditions to be considered forms of vasculitis.
The exact cause of Majocchi's granuloma is not well established however a dysfunctinoal immune system may be a causative factor. The first form of MG, the superficial perifollicular form occurs predominately on the legs of otherwise healthy young women who repeatedly shave their legs and develop hair follicle occlusions that directly or indirectly disrupt the follicle and allow for passive introduction of the organism into the dermis. Hence, the physical barrier of the skin is important because it prevents the penetration of microorganisms. Physical factors that play a major role in inhibiting dermal invasion include the interaction among keratin production, the rate of epidermal turnover, the degree of hydration and lipid composition of the stratum corneum, CO levels, and the presence or absence of hair. Keratin and/or necrotic material can also be introduced into the dermis with an infectious organism to further enhance the problem. In immunocompromised individuals, the use of topical corticosteroids may lead to a dermatophyte infection due to local immunosuppression.
Non-blanching rash (NBR) is a medical term used to describe a skin rash that does not fade when pressed with, and viewed through, a glass.
It is a characteristic of both purpuric and petechial rashes. Individual purpura measure 3–10 mm (0.3–1 cm, - in), whereas petechiae measure less than 3 mm.
A non-blanching rash can be a symptom of bacterial meningitis, but this is not the exclusive cause.
Waldenström hyperglobulinemic purpura (also known as "Purpura hyperglobulinemica") is a skin condition that presents with episodic showers of petechiae (small red or purple spots) occurring on all parts of the body, most profusely on the lower extremities.
Hemosiderin hyperpigmentation is pigmentation due to deposits of hemosiderin, and occurs in purpura, hemochromotosis, hemorrhagic diseases, and stasis dermatitis.
Majocchi's disease (also known as Majocchi's Granuloma, "Purpura annularis telangiectodes,", and "Purpura annularis telangiectodes of Majocchi") is well-recognized but uncommon skin condition characterized by purple/bluish-red 1- to 3-cm annular patches composed of dark red telangiectases with petechiae. The name Majocchi's comes from the Professor Domenico Majocchi who first discovered the disorder in 1883. Domenico Majocchi was a professor of dermatology at the University of Parma and later the University of Bologna. Majocchi's disease can be defined as an infection of the dermal and subcutaneous tissues due to a fungal mold infection on the cutaneous layer of the skin. The most common dermatophyte is called "Trichophyton rubrum." This disease can affect both immunocompetent and immunocompromised hosts. However, immunocompromised individuals have a higher risk.
Cryofibrinogenemic purpura is a skin condition that manifests as painful purpura with slow healing ulcerations and edema of both feet during winter months.
Nonthrombocytopenic purpura is a type of purpura (red or purple skin discoloration) not associated with thrombocytopenia.
Examples/causes include:
- Henoch–Schönlein purpura.
- Hereditary hemorrhagic telangiectasia
- Congenital cytomegalovirus
- Meningococcemia
Treat the underlying disease . Eg for wegner's treatment is steroids and cyclophosphamide.
Urticaria is a vascular reaction of the skin characterized by the appearance of wheals, which are firm, elevated swelling of the skin. Angioedema, which can occur alone or with
urticaria, is characterized by a well-defined, edematous swelling that involves subcutaneous tissues, abdominal organs, or upper airway.
- Acquired C1 esterase inhibitor deficiency
- Acute urticaria
- Adrenergic urticaria
- Anaphylaxis
- Aquagenic urticaria
- Cholinergic urticaria
- Chronic urticaria (ordinary urticaria)
- Cold urticaria
- Dermatographism (dermographism)
- Episodic angioedema with eosinophilia (Gleich's syndrome)
- Exercise urticaria (exercise-induced urticaria)
- Galvanic urticaria
- Heat urticaria
- Hereditary angioedema (Quincke's edema)
- Localized heat contact urticaria
- Mast cell-independent urticaria
- Physical urticaria
- Primary cold contact urticaria
- Pressure urticaria (delayed pressure urticaria)
- Reflex cold urticaria
- Schnitzler syndrome
- Secondary cold contact urticaria
- Solar urticaria
- Systemic capillary leak syndrome
- Urticarial allergic eruption
- Urticaria-like follicular mucinosis
- Vibratory angioedema
Purpura is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure. The spots are caused by bleeding underneath the skin usually secondary to vasculitis or dietary deficiency of vitamin C (scurvy). They measure 0.3–1 cm (3–10 mm), whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm.
Purpura is common with typhus and can be present with meningitis caused by meningococci or septicaemia. In particular, meningococcus ("Neisseria meningitidis"), a Gram-negative diplococcus organism, releases endotoxin when it lyses. Endotoxin activates the Hageman factor (clotting factor XII), which causes disseminated intravascular coagulation (DIC). The DIC is what appears as a rash on the affected individual.
Ionizing radiation-induced cutaneous conditions result from exposure to ionizing radiation.
- Acute radiodermatitis
- Chronic radiation keratosis
- Chronic radiodermatitis
- Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy
- Fluoroscopy burn
- Radiation acne
- Radiation cancer
- Radiation dermatitis (radiodermatitis)
- Radiation recall reaction
- Radiation-induced erythema multiforme
- Radiation-induced hypertrophic scar
- Radiation-induced keloid
- Radiation-induced morphea
Gougerot–Blum syndrome (also known as "pigmented purpuric lichenoid dermatitis", and "pigmented purpuric lichenoid dermatitis of Gougerot and Blum") is a variant of pigmented purpuric dermatitis, a skin condition characterized by minute, rust-colored to violaceous, lichenoid papules that tend to fuse into plaques of various hues. Relative to other variants, it is characterized clinically by a male predominance, pruritus, with a predilection for the legs, and histologically, it features a densely cellular lichenoid infiltrate.
It was characterized in 1925.
Gougerot–Blum syndrome is named after the French dermatologists Henri Gougerot (1881–1955) and Paul Blum (1878–1933).
Cutaneous vasculitis can have various causes including but not limited to medications, bacterial and viral infections or allergens. It is estimated that 45-55% of cases are idiopathic, meaning the cause is unknown. In cases where a cause can be determined, medications and infectious pathogens are most common in adults, while IgA vasculitis (Henoch-Schönlein purpura) frequently affects children. Other etiologies include autoimmune conditions and malignancies, usually hematologic (related to the blood).
The small vessels in the skin affected are located in the superficial dermis and include arterioles (small arteries carrying blood to capillaries), capillaries, and venules (small veins receiving blood from capillaries). In general, immune complexes deposit in vessel walls leading to activation of the complement system. C3a and C5a, proteins produced from the complement system, attract neutrophils to the vessels. Once activated, neutrophils then release preformed substances, including enzymes causing damage to vessel tissue. Evidence of this process can be seen with a sample of removed skin tissue, or biopsy, viewed under a microscope. Neutrophils are seen surrounding blood vessels and their debris within vessel walls, causing fibrinoid necrosis. This finding on histological examination is termed “leukocytoclastic vasculitis”.
Considering the wide range of potential causes leading to cutaneous small vessel vasculitis, there are subtle variations in the underlying pathophysiology for each cause. For example, medications are metabolized to smaller molecules that can attach to proteins in the blood or vessel walls. The immune system senses these altered proteins as foreign and produces antibodies in efforts to eliminate them from the body. A similar process occurs with infectious agents, such as bacteria, in which antibodies target microbial components.
Palpable purpura is a condition where purpura, which constitutes visible non-blanching hemorrhages, are raised and able to be touched or felt upon palpation. It indicates some sort of vasculitis secondary to a serious disease.
In most cases skin lesions do not cause symptoms, however itching, burning, or pain may occur.
Frequently reported symptoms include mild fever, muscle pain, joint pain, or an overall feeling of discomfort. Additional symptoms depend on the cause of the vasculitis and if other organ systems are involved. For example, if the vasculitis is a manifestation of Henoch-Schönlein purpura, individuals may also experience abdominal pain or blood in the urine.
Telangiectasia macularis eruptiva perstans is persistent, pigmented, asymptomatic eruption of macules usually less than 0.5 cm in diameter with a slightly reddish-brown tinge.
Purpura are a common and nonspecific medical sign; however, the underlying mechanism commonly involves one of:
- Platelet disorders (thrombocytopenic purpura)
- Primary thrombocytopenic purpura
- Secondary thrombocytopenic purpura
- Post-transfusion purpura
- Vascular disorders (nonthrombocytopenic purpura)
- Microvascular injury, as seen in senile (old age) purpura, when blood vessels are more easily damaged
- Hypertensive states
- Deficient vascular support
- Vasculitis, as in the case of Henoch–Schönlein purpura
- Coagulation disorders
- Disseminated intravascular coagulation (DIC)
- Scurvy (vitamin C deficiency) - defect in collagen synthesis due to lack of hydroxylation of procollagen results in weakened capillary walls and cells
- Meningococcemia
- Cocaine use with concomitant use of the one-time chemotherapy drug and now veterinary deworming agent levamisole can cause purpura of the ears, face, trunk, or extremities, sometimes needing reconstructive surgery. Levamisole is purportedly a common cutting agent.
- Decomposition of blood vessels including purpura is a symptom of acute radiation poisoning in excess of 2 Grays of radiation exposure. This is an uncommon cause in general, but is commonly seen in victims of nuclear disaster.
Cases of psychogenic purpura are also described in the medical literature, some claimed to be due to "autoerythrocyte sensitization". Other studies suggest the local (cutaneous) activity of tissue plasminogen activator can be increased in psychogenic purpura, leading to substantial amounts of localized plasmin activity, rapid degradation of fibrin clots, and resultant bleeding. Petechial rash is also characteristic of a rickettsial infection.
Pigmented warts are a cutaneous condition commonly reported in Japan, most often occurring on the hands or feet.
The condition was originally considered characteristic of rubella, but is now considered to be potentially associated with many other conditions, such as cytomegalovirus and metastatic neuroblastoma.
Ultraviolet light from the sun causes premature aging of the skin and skin damage that can lead to melanoma. Some scientists hypothesize that overexposure to UV, including excessive sunlight, may play a role in the formation of acquired moles. However, more research is needed to determine the complex interaction between genetic makeup and overall exposure to ultraviolet light. Some strong indications that this is so (but falling short of proof), are:
- The relative lack of moles on the buttocks of people with dysplastic nevi.
- Freckles (spots of melanin on the skin, and distinct from moles) are known to be influenced by sunlight.
Studies have found that sunburns and too much time in the sun can increase the risk factors for melanoma. This is "in addition to" those who have dysplastic nevi being at higher risk of this cancer (the uncertainty is in regard to acquiring "benign" moles). To prevent and reduce the risk of melanoma caused by UV radiation, the American Academy of Dermatology and the National Cancer Institute recommends staying out of the sun between 10 a.m. and 4 p.m. standard time (or whenever one's shadow is shorter than one's height). The National Cancer Institute also recommends wearing long sleeves and trousers, hats with a wide brim, sunscreens, and sunglasses that have UV-deflecting lenses.