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)

Most skin diseases associated with swimming are relatively minor and either heal spontaneously or respond quickly to treatment. Exceptions are those diseases made worse by sunlight such as lupus erythematosus, skin cancer, or prematurely aged skin. With the use of better sunscreens in the future, that problem will be solved.
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PMID:Swimming and the skin. 32 58

Fourteen cases of multifocal squamous cell cancer of the skin are analyzed clinicomorphologically. Such form of skin cancer arises typically on the limbs following long-standing lesions: trophic ulcer, osteomyelitis, psoriasis, lupus. The tumors are both synchronous and metachronous. The prognosis is often unfavorable due to late diagnosis. Multiplicity of the lesions could be attributed to lymphogenic or hematogenic subcutaneous metastases in generalization of the malignant process.
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PMID:[Multiple-primary cancer of the skin]. 177 25

Skin affected by a burn cancer is scarred, ulcerated, and often appears as erythema ab igne clinically in adjacent skin. The latent period in burn scar malignancy is much longer for SCC than BCC. Malignant melanoma and various sarcomas are reported to arise in burn scars, too. The other extreme on the temperature scale can less often result in enough permanent acral damage that poor wound healing may eventually result in cancer, usually SCC. About 1% of patients with chronic osteomyelitis develop cancer, usually SCC in sinus tracts. As with tumors arising in burn scars and chronic leg ulcers of varied etiology, black patients are disproportionately overrepresented in osteomyelitic malignancy. In nearly all of the patients with radiation-induced skin cancer, concomitant radiodermatitis is present. As with burn scar and osteomyelitic cancer, x-ray related cancer has a long latent period. Similar to burn scar cancer, SCC predominates in osteomyelitis and occurs on the extremities. BCC, when it arises, is more common on the face and neck in burn- and radiation-induced tumors. Multiple tumors are frequent as is recurrence in x-ray malignancy. Mortality is high: one out of three to four patients with burn scar, osteomyelitic, and radiation cancer die of dermatosis-related malignancy. Recently, radioactivity-contaminated gold rings have been implicated in causing SCC. Carcinoma tends to occur in irradiated benign dermatoses whereas sarcomas tend to complicate irradiated malignancies. Stasis ulceration and anogenital fistulae may rarely lead to cancer, SCC in the former and adenocarcinoma in the latter. SCC can rarely develop in four related conditions (acne conglobata, dissecting perifolliculitis of the scalp, hidradenitis suppurativa, and pilonidal sinus) after a lengthy latent period; prognosis is poor with a high metastatic rate. A whole host of chronic cutaneous infections can lead to malignancy occasionally; these include lupus vulgaris, lymphogranuloma veverum, granuloma inguinale, leprosy, actinomycosis, and candidiasis. BCC more than SCC is known to complicate smallpox vaccination sites. Certain erosive and/or scarring dermatoses other than those mentioned above can be unusually affected by secondary malignancy. Discoid lupus erythematosus lesions often subjected to the carcinogenic effects of sunlight can degenerate into SCC in patients with either light or dark skin. In acrodermatis chronica atrophicans, a condition not often seen in the United States, the involved skin, particularly of the lower extremities, is susceptible to SCC, lymphoma, and BCC. Epidermolysis bullosa, especially the recessive dystrophic variant, can be complicated by SCC on affected mucous membrane and acral skin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cancer complicating chronic ulcerative and scarifying mucocutaneous disorders. 307 55

In vivo ultraviolet (UV) exposure of human skin abrogates the antigen-presenting function of T6+ DR+ Langerhans cells and induces the appearance of antigen-presenting T6- DR+ epidermal melanophages. UV-exposed epidermal cells containing T6- DR+ epidermal antigen-presenting cells, in contrast to unexposed epidermal cells containing T6+ DR+ Langerhans cells, potently activate autoreactive regulatory T cells in the absence of exogenous antigens. Autoreactive T cells may be important for regulation of other immune responses such as those which occur in photosensitive lupus erythematosus and in immune surveillance of UV-induced skin cancers. It is therefore imperative to determine the factors that govern their appearance in the skin. It was found that UVB and UVC, but not UVA, induced a dose-dependent appearance of T6- DR+ epidermal melanophages. The optimal time of appearance was 2 or 3 days after UVB and UVC exposure. In contrast, UVA was a poor inducer of T6- DR+ cells at all doses and all time points tested. Although UVA was a poor inducer of T6- DR+ epidermal cells, UVA radiation resulted in depletion of T6+ DR+ Langerhans cells from the epidermis, as did UVB and UVC radiation. This differential effect of UV wave bands on the immunocompetent cells in human skin may be related to the greater potential of UVB exposure to induce skin cancers and to exacerbate systemic lupus erythematosus.
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PMID:Dose response and time course for induction of T6- DR+ human epidermal antigen-presenting cells by in vivo ultraviolet A, B, and C irradiation. 350 Jan 91

Skin cancer is relatively uncommon among black individuals. Squamous cell carcinoma occurred in a scar of chronic discoid lupus erythematosus in a black patient. A review of 7 previously reported cases of squamous cell carcinoma in blacks with chronic discoid lupus erythematosus indicates a tendency of the cancer to metastasize. Sun exposure of the hypopigmented lesions of chronic discoid lupus and possibly other factors predispose to cancer of the skin. Poorly healing skin lesions in chronic discoid lupus should arouse suspicion of malignant change.
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PMID:Squamous cell carcinoma of the skin in black patients with discoid lupus erythematosus. 357 18

Chronic sun exposure has been linked to induction of skin cancers including melanoma and aging changes of the skin, has an adverse effect on certain diseases such as lupus erythematosus and is responsible for drug-induced phototoxic reactions. A majority of an individual's lifetime sun exposure may occur during childhood, and thus early photoprotection is desirable. We conducted a written survey of Florida pediatricians regarding their inclusion of sun protection information as part of routine well-child care. The results indicated that a majority of the pediatricians have awareness of the need for parent and patient education about sun-related issues, and most (65%) requested further information and educational materials. This study suggests that expanded educational efforts concerning sun-related health hazards and sun protection would be desirable for physicians involved in pediatric care, for parents, and for children.
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PMID:Sun protection in well-child care: results of a survey of Florida pediatricians. 380 23

A bright, continuous, granular deposition of immunoreactants at the dermo-epidermal junction (DEJ) of lesional skin is highly suggestive of cutaneous lupus erythematosus (LE). A recent study of the direct immunofluorescence (IF) of sun-exposed skin in normal adults has demonstrated findings similar to the bright, continuous granular pattern found in cutaneous LE. This data suggests that positive IF from sun-exposed cutaneous lupus lesions is nonspecific. Forty-one healthy adults, without a history of dermatoses or photosensitivity, presenting to the dermatology clinic for the excision of skin cancers were studied. Excess non-lesional tissue, removed from Moh's excision sites (sun-exposed face and neck) in order to obtain appropriate cosmetic closure, was examined for the deposition of immunoreactants. The specimens were incubated with fluoresceinated monovalent anti-human immunoglobulin specific for IgG, IgA, IgM, C3, Clq, and fibrinogen and examined independently by 2 immunodermatologists without prior knowledge of patient or site. None of the samples demonstrated immunoreactant deposition consistent with cutaneous LE. IF of several specimens (21/41) had a weak (1+ or 2+), interrupted pattern of fibrinogen at the DEJ,--a common, non-specific finding. Weak, interrupted, linear and granular patterns were seen with IgM (10/41), Clq (9/41), IgG (2/41), IgA (2/41), and C3 (1/41). Fibrinogen was the only immunoreactant demonstrating a bright (3+), continuous, granular pattern (4/41). This data suggests that sun-exposure alone does not induce the deposition of immunoreactants at the DEJ in a pattern similar to that found in cutaneous LE.
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PMID:Occurrence of positive immunofluorescence in the dermo-epidermal junction of sun-exposed skin of normal adults. 796 22

Irradiation with ultraviolet B (UVB; 290-320 nm) initiates systemic immunosuppression of contact hypersensitivity (CHS). UV dose-responses for suppression of CHS to trinitrochlorobenzene were established in 18 strains of inbred mice. Three phenotypes with significantly different susceptibilities to UV suppression were identified. The phenotypes were: high (HI) susceptibility, 50% suppression with 0.7-2.3 kJ/m2 UV (C57BL/6, C57BL/10, and C57L and NZB females); low (LO) susceptibility, 50% suppression with 9.6-12.3 kJ/m2 UV (BALB/c, AKR, SJL and NZW), and intermediate (INT) susceptibility, 50% suppression with 4.7-6.9 kJ/m2 UV (DBA/2, C57BR, C3H/HeJ, C3H/HeN, CBA/N and A/J). UV suppression was not correlated with skin pigmentation or with the magnitude of the CHS response in non-irradiated animals. Major histocompatibility complex (MHC) haplotype was not correlated with UV suppression in MHC congenic strains B10.D2/oSnJ, B10.D2/nSnJ, B10.BR/SgSnJ, and A.BY/SnJ. There were no sex differences in UV suppression in BALB/c, C57BL/6, or NZW animals. In the autoimmune NZB strain, however, male mice (LO) were seven times less sensitive to UV suppression than NZB female mice (HI). Both sexes of (NZB x NZW)F1 and (NZW x NZB)F1 mice were HI, supporting dominance of HI over LO. Thus there are genetic factors and interacting sex-limited factors determining susceptibility to UV suppression. These findings may be of relevance to UV-related diseases such as photosensitive lupus and skin cancer.
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PMID:Susceptibility to immunosuppression by ultraviolet B radiation in the mouse. 822 36

In the present literature there is still controversy as to whether patients with systemic lupus erythematosus (SLE) are at increased risk of developing malignant diseases. In recent years a number of epidemiological studies have been conducted and some have suggested an association between SLE and malignant diseases while other studies have not. The objective of this study was to investigate this relationship in an unselected cohort of Icelandic patients with SLE. All patients diagnosed with SLE registered in the Icelandic SLE database were compared to the Icelandic cancer registry. For completeness, hospital charts and outpatient notes were also reviewed. The study period was from 1957 to the end of 2001. The O/E (observed/expected ratio), CI and P-value were calculated for total number of malignancies as well as individual malignancy types. Of 238 patients diagnosed with SLE (213 women and 25 men) 39 malignancies were diagnosed in 36 patients; 32 women and four men. Of the 36 patients, 27 were diagnosed subsequently with SLE and malignant disease. The mean age at diagnosis of SLE was 43.2 years (range 10-81) and at time of diagnosis of malignancy 62.7 years (range 43-86). The O/R for the whole study population was 1.38 (CI 0.89-1.87, P = 0.063), 1.45 for the women (CI 0.91-1.99, P = 0.051) and 1.03 for the men (CI 0.22-2.66, P = 0.560). The O/R for the most frequent malignancies diagnosed subsequently to SLE was 6.43 for squamous cell skin cancer (CI 1.31-18.5, P = 0.012), 5.48 for lymphoma (CI 0.64-19.6, P = 0.052), 2.46 for uterine cancer (CI 0.29-8.78, P = 0.196), 2.0 for ovarian cancer (CI 0.23-7.14, P = 0.264), 1.72 for lung cancer (CI 0.36-4.95, P = 0.254) and 1.6 for breast cancer (CI 0.65-3.23, P = 0.154). The total number of patient-years at risk was 2774 years. The results from this study on an unselected cohort of Icelandic SLE patients do not suggest an overall association between SLE and malignancy. Squamous cell skin cancer was the only individual cancer type that was statistically increased in the population and the numbers for lymphoma were borderline statistically significant.
Lupus 2003
PMID:Risk of malignancy in an unselected cohort of Icelandic patients with systemic lupus erythematosus. 1451 31

Antigen-specific CD8+T lymphocytes play an important role in defense against cutaneous microbial infection and skin cancer as well as in the pathophysiology of autoimmune skin disease such as lupus erythematodes and vitiligo. We have explored the role of CD8+ cytotoxic T lymphocytes (CTL) in an experimental mouse model of vitiligo, a pigmentation disorder characterized by focal loss of melanocytes in the skin. Using genetic immunization techniques we found that pigment cells in the epidermis can be destroyed by CD8+ T cells specifically recognizing a single H2-Kb-binding peptide derived from the model melanocytic self antigen tyrosinase-related protein 2 (TRP2), a melanosomal enzyme involved in pigment synthesis. Experimental evidence suggests that peripheral tolerance of pigment cell-specific cytotoxic CD8+T cells is regulated in two steps. In the induction phase, stimulation and expansion of these T cells in vivo strictly depends on CD4+ T cell help. In the effector phase, autoimmune destruction of melanocytes in the skin depends on local inflammation facilitating the migration of T cells into the epidermis and supporting effector functions. Our results suggest that accidental stimulation of CD8+ CTL recognizing MHC class I-binding peptides derived from melanocytic proteins in the context of an inflammatory skin disease may play an important role in the pathophysiology of vitiligo. Further investigations will address the role of chemokines, chemokine receptors and adhesion molecules in this experimental system and will reveal the role of keratinocytes and Langerhans cells in regulating cutaneous CD8+ T cell responses.
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PMID:Initiation and regulation of CD8+T cells recognizing melanocytic antigens in the epidermis: implications for the pathophysiology of vitiligo. 1567 23


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