Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of the lupus erythematosus results from co-operation of three principles: (1) genetical disposition, (2) increased reactivity of the immune system, (3) different exogenic influences. The genetical disposition is confirmed by family investigations, metabolic disorders and immune anomalies as well as by parallels to animal models. The reaction manner of the immune system is genetically determined. Exogenic factors influence the immune system (behaviour) either as starter or by modifying the genetical material. The most striking humoral immune phenomenon is an immense number of (auto-)antibodies. Investigations of xeroderma pigmentosum as well as with DNA of different antigenity have shown that an increase of the antigenicity is unlikely for this phenomenon. In the serum of patients there were established and partially characterized factors (mitogens, granulocytic adherence-factor) for increasing the immune reactivity. The increase of such factors may be the sequence of a T-suppressor cell-defect. Like-wise no interdigitating cells in systemic lupus erythematosus have been found, cells which may be responsible for the terminal differentiation of T-lymphocytes. The mode of action of exogenic factors is represented and discussed with the example of the UV provocation.
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PMID:[New studies on the pathogenesis of lupus erythematosus]. 9 93

Skin diseases associated with photosensitivity are numerous and may be divided into three main groups: photo-aggravated dermatoses, genophotodermatoses and metabolic photodermatoses. Photo-aggravated dermatoses are autonomous skin diseases in which exposure to sunlight may make the disease worse or precipitate its onset and/or its progressiveness; this group includes lupus erythematosus, autoimmune bullous diseases, acantolytic dyskeratoses, acne vulgaris, rosacea and cutaneous lymphoid infiltrates. To these must be added photosensitive forms of autonomous dermatoses such as atopic dermatitis, psoriasis, herpes labialis, erythema multiforme, granuloma and disseminated superficial actinic porokeratosis. Genophotodermatoses are genodermatoses which are made photosensitive by a recognized or as yet unidentified deficiency of the natural photoprotection system. In this group are albinism, vitiligo, xeroderma pigmentosum and poikiloderma. Metabolic photodermatoses are diseases in which photosensitization reactions, often revealing, are due to the accumulation in the skin of an endogenous chromophore as a result of a congenital (porphyria) or acquired (pellagra) enzymatic disorder.
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PMID:[Skin diseases with photosensitivity]. 152 48

The authors present a new classification for photodermatosis in five groups: 1. Primary toxic photodermatosis that means lesions produced in all human beings by non-ionized radiation. 2. Photodermatosis induced by drugs, with two subgroups--phototoxic and photoalergic--according to the mechanism of action of the drug. 3. Idiopathic photodermatosis in which the photonic effects are known but the chromophores are unknown; four conditions are included here polymorphous actinic eruption, solar urticaria, actinic reticuloid and hidroa vacciniforme. 4. Miscelanea group which includes several conditions of unknown mechanism which are not included in the other groups, such as: actinic cheilitis, actinic poikiloderma, actinic ceratoses, epitheliomas, melanomas and others. 5. Conditions precipitated or aggravated by solar radiation with two sub-groups: hereditary (xeroderma pigmentosum, Hartnup's syndrome and other) and acquired (lupus erythematosus, pellagra and other). In group 1, the authors propose the designation of actinic elastotic dermatosis to unify different conditions described by several authors such as: diffuse elastosis, citrein skin, cutis rhomboidalis, and others.
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PMID:[A new classification of photodermatoses]. 266 86

Photosensitivity diseases are reviewed. The pathogenesis of photodermatoses is not completely elucidated, especially because the photosensitizing agents are rarely identified. In exogenous photosensitization, the chemical agent (chromophore) is most often identified, reaching the skin either via topical contact or by systemic administration (drugs). Concepts of phototoxicity (photochemical reaction) and photo-allergy (photo-immunologic reaction) explain the clinical aspects. Dermatoses with photosensitivity are divided into three groups: photo-aggravated dermatoses (solar herpes, lupus erythematosus), photosensitivity caused by protective system defect (xeroderma pigmentosum), and photosensitivity caused by metabolic defects (porphyrias, pellagra). Idiopathic photodermatoses (unknown chromophore) are triggered by solar exposure (systemic photo-allergens would serve as mediators): 'benign estival polymorphous light eruption', polymorphous light eruptions, persistent light reactor, solar urticaria.
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PMID:[Photosensitivity in human pathology: mechanisms and clinical aspects]. 309 82

Instrumentation for studying action spectra in controls and various light-associated diseases is described. This study summarizes tests performed with a prism grating monochromator during the last 10 yr. There were 68 photodermatoses studied: xeroderma pigmentosum (XP) (1), lupus erythematosus (LE) (12), polymorphous light eruption (PLE) (23), solar urticaria (4), actinic reticuloid (2), halogenated salicylanilide photosensitivity and persistent light reactors (11), psoralen photosensitivity (6), and porphyria (9). A normal minimal erythema dose in the UVB (below 320 nm) was generally observed in polymorphous light eruption and lupus erythematosus. The most exquisite photosensitivity for delayed erythema was observed in actinic reticuloid, which in one case was 25-35 times more sensitive in the UVB range which was also observed but to a lesser extent in XP and in persistent light reactors. Persistence of erythema and edema at test sites was observed in XP, PLE, LE, and actinic reticuloid. A delay in development of erythema reaching a maximum at 72 hr was observed in XP and psoralen phototoxicity. Maximum photosensitivity occurred in solar urticaria. Three patients had peak sensitivity in the range of 310-313 nm and the 4th at 460 nm. Photosensitivity in the visible range was detected in 2 patients with solar urticaria, one with actinic reticuloid, and confirmed in 9 patients with porphyria (405 nm). Photosensitivity in the UVA (above 320 nm) occurred to some degree in all groups.
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PMID:Instrumentation and action spectra in light-associated diseases. 725 55

Photosensitivity in the pediatric patient is caused by a diverse group of disorders. It may indicate a serious underlying systemic disease such as lupus erythematosus or dermatomyositis, or be an early symptom of a rare group of genetic disorders that includes the porphyrias, xeroderma pigmentosum, Cockayne syndrome, Bloom syndrome, and Rothmund-Thomson syndrome. Idiopathic disorders and ultraviolet light-induced reactions to topical or systemic agents may also cause photosensitivity in children. Early recognition and prompt diagnosis may prevent complications associated with prolonged unprotected exposure to sunlight and permit recognition of families at risk for rare heritable disorders associated with photosensitivity.
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PMID:Photosensitivity in the pediatric patient. 930 Jan 96

A connection between vitamin D deficiency and severe health problems including various types of cancer has been demonstrated. We have shown that patients that have to protect themselves against solar UV radiation for medical reasons, including patients with xeroderma pigmentosum (XP), basal cell nevus syndrome (BCNS), lupus erythematodes (LE) or transplant recipients, are at risk to develop vitamin D deficiency. We conclude that 25-hydroxyvitamin D serum levels as a measure of vitamin D status have to be analyzed in patients that have to protect themselves against solar UV radiation for medical reasons. Suboptimal vitamin D status has to be substituted (e.g. via oral treatment) to protect against serious vitamin D deficiency-related health problems without increasing the risk to develop solar UV-induced skin cancer. Our finding that protection against solar UV radiation causes vitamin D deficiency underlines the need for re-defining dermatological recommendations for solar UV protection in skin cancer prevention programs.
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PMID:Sunlight, skin cancer and vitamin D: What are the conclusions of recent findings that protection against solar ultraviolet (UV) radiation causes 25-hydroxyvitamin D deficiency in solid organ-transplant recipients, xeroderma pigmentosum, and other risk groups? 1720 18

Ultraviolet radiation (UVR) is hazardous to patients with photosensitive skin disorders, such as lupus erythematosus, xeroderma pigmentosum and skin cancer. As such, these patients are advised to minimize their exposure to UVR. Classically, this is accomplished through careful avoidance of sun exposure and artificial tanning booths. Indoor light bulbs, however, are generally not considered to pose significant UVR hazard. We sought to test this notion by measuring the UV emissions of 19 different compact fluorescent light bulbs. The ability to induce skin damage was assessed with the CIE erythema action spectrum, ANSI S(lambda) generalized UV hazard spectrum and the CIE photocarcinogenesis action spectrum. The results indicate that there is a great deal of variation amongst different bulbs, even within the same class. Although the irradiance of any given bulb is low, the possible daily exposure time is rather lengthy. This results in potential daily UVR doses ranging from 0.1 to 625 mJ cm(-2), including a daily UVB (290-320 nm) dose of 0.01 to 15 mJ cm(-2). Because patients are exposed continually over long time frames, this could lead to significant cumulative damage. It would therefore be prudent for patients to use bulbs with the lowest UV irradiance.
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PMID:Analysis of compact fluorescent lights for use by patients with photosensitive conditions. 1932 Aug 50

Photosensitivity in childhood is caused by a diverse group of diseases. A specific sensitivity of a child's skin to ultraviolet light is often the first manifestation or a clinical symptom of photodermatosis. It might indicate a serious underlying systemic disease such as lupus erythematosus or dermatomyositis, or a rare group of genetic skin disorders like Xeroderma pigmentosum, Cockayne syndrome, Trichothyodystrophy, Bloom syndrome, Rothmund-Thomson and Kindler syndrome as well as metabolic disorders and cutaneous porphyria. Photosensitivity secondary to topical or systemic agents may also cause photosensitivity in children. Early recognition and prompt diagnosis may prevent complications associated with unprotected exposure to sunlight and avoid actinic injuries that can lead to malignant skin changes.
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PMID:Photosensitivity skin disorders in childhood. 2130 30