Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The porphyrias are the only group of diseases caused by endogenous phototoxic agents. While patients with erythropoietic protoporphyria and those with porphyria cutanea tarda both have skin lesions on sun-exposed areas, there are differences in their cutaneous manifestations. Based on information discussed in this chapter, the following pathophysiologic mechanisms can be proposed. In porphyria cutanea tarda, photoactivation of the complement system in the presence of uroporphyrin results in activation of dermal mast cells, which release their proteases. This results in dermal-epidermal separation, reflected clinically as skin fragility and vesicles. The interaction between activated mast cells with fibroblasts, the nature of which is still unclear, may contribute to fibrosis and sclerodermoid skin changes. The stimulatory effect of uroporphyrin on collagen biosynthesis by fibroblasts, which occurs independent of irradiation, may be responsible for the sclerodermoid lesions seen at sun-exposed as well as sun-protected areas. In erythropoietic protoporphyria, mast cell activation can occur as the result of complement activation induced by protoporphyrin and irradiation. Protoporphyrin and irradiation may also directly induce the release of preformed and generated mediators from mast cells, a process mediated at least in part by peroxidation. The release of mast cell mediators may account for the erythema, edema, and urticaria observed in patients with erythropoietic protoporphyria upon exposure to sunlight. Interaction of mast cells with fibroblasts, and the direct membrane-damaging effect of protoporphyrin and irradiation on the latter, may contribute to the waxy thickening of skin seen in chronically sun-exposed areas of these patients. There are, however, many unanswered questions. What accounts for the different biological effects of mast cell-derived mediators: dermal-epidermal separation in one, erythema and urticaria in the other? The fragmentation of dermal collagen bundles associated with cleavage beneath the lamina densa, and the hyperpigmentation and hypertrichosis observed in some patients with porphyria cutanea tarda remain unexplained. What is the mechanism of the reduplication of blood vessel basal lamina in the non-sun-exposed areas of both types of patient? Are there any roles for cytokines and epidermal cell-derived eicosanoids? While it is clear that the pathogenesis of cutaneous lesions in porphyria cutanea tarda and erythropoietic protoporphyria involves interactions among inflammatory mediators and various cells in skin, much still needs to be done to further our understanding of their pathophysiology.
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PMID:Mechanisms of phototoxicity in porphyria cutanea tarda and erythropoietic protoporphyria. 248 74

The porphyrias can be grouped conveniently by their presenting symptoms. Acute intermittent neurological symptoms of neuritis, abdominal pain and psychoses may occur in acute intermittent porphyria, hereditary coproporphyria and variegata porphyria. Increase of the porphyrin precursors delta-aminolaevulinic acid and porphobilinogen may be observed in the urine during attacks (Watson-Schwartz test). Patients with acute symptoms of photosensitivity with burning pain and oedema within short exposure periods may have erythropoietic protoporphyria, with high erythrocyte and stool protoporphyrins, erythropoietic coproporphyria, and in the last few years of life the more recently described hepatoerythropoietic porphyria. Symptoms of chronic photosensitivity include; hyperpigmentation, hypertrichosis, easy fragility of the skin with bullae and subsequent scarring in porphyria cutanea tarda (PCT), with increased uroporphyrin in the urine and stool; variegate porphyria with increased protoporphyrin and coproporphyrin in the stool; congenital erythropoietic porphyria with an increased copro- and uroporphyrin (isomer I) in the erythrocytes, urine and stool; and hepatoerythropoietic porphyria in later life, in which the chronic features are similar to PCT. In 1913 Meyer-Betz injected himself with 200 mg haematoporphyrin. Initially, at the higher levels, the symptoms were those of solar urticaria as observed in erythropoietic porphyria, but after several months became identical to PCT. A comparison of quantitative porphyrin analysis (performed on 323 patients with porphyria) and chromatography provides additional confirmation for the diagnosis.
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PMID:Porphyria: genetic and acquired. 329 37

Sporting activities may exert positive and negative health effects. This applies not only to the cardiovascular and musculoskeletal system, but also to skin. During sporting activities a person is exposed to environmental factors such as temperature, irradiation, and allergens. These factors may play a key role in the development of skin diseases. Mechanical trauma is caused by acute injury as well as chronic damage. Infectious skin diseases caused by viruses, bacteria or fungi can be transmitted by body contact or the use of communal showers or locker rooms. Intake of performance-enhancing substances may provoke skin changes such as striae distensae, androgenetic alopecia, hypertrichosis and acne. Preexisting skin diseases such as psoriasis, lichen planus, vitiligo, polymorphous light eruption, lupus erythematosus, porphyria, urticaria, and acne rosacea may be aggravated by sporting activities. On the other hand, physical exercise has a therapeutic potential which has hardly been exploited by dermatologists. Especially in chronic skin diseases positive effects have been observed. Therapeutic use of team sports has been shown to decrease suffering, depression, and emotional disturbances and increase life quality in patients with atopic eczema, psoriasis, and venous leg ulcers.
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PMID:[Sports as a risk factor and therapeutic principle in dermatology]. 1196 1

Selective seritonin reuptake inhibitors (SSRIs) are widely used antidepressants that are often safer than alternatives, but may produce a variety of cutaneous reactions including spontaneous bruising, pruritus, urticaria, angioedema, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, erythema nodosum, alopecia, hypertrichosis, leukocytoclastic vasculitis, and an acneiform eruption. We review this category of medications and its side effects. Many cutaneous alterations seen in association with SSRIs can be serious, some even life threatening. Because there appears to be cross-reactions between SSRIs, even though they have different chemical structures, it is advisable to use another family of antidepressants if an SSRI is linked with a serious skin eruption.
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PMID:Cutaneous effects of the most commonly used antidepressant medication, the selective serotonin reuptake inhibitors. 1714 71