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)

We examined 104 patients divided in two groups: patients suffering from lupus erythematosus systemic (SLE) and from lupus erythematosus cutaneous (CLE). Cellular immunity tests in vivo were performed in all patients: DNCB, PPD, Trichophytin, Candidin. Cellular immunity response were compared according to undergoing steroid therapy. Patients suffering from CLE had decreased reaction to cellular immunity test with increased dose of steroid therapy. In patient with SLE this decrease was not recognised.
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PMID:[The effect of steroid therapy on cellular reactions in vivo in patients with cutaneous and systemic forms of erythematosus]. 262 66

We studied in vitro spontaneous and ultraviolet light (UV)-induced lymphocyte apoptosis in patients with systemic lupus erythematosus (SLE, n = 11), cutaneous lupus erythematosus (CLE, n = 8), and other collagen diseases (n = 6), as well as normal individuals (n = 6). Apoptosis was confirmed by the presence of a 180 bp DNA ladder on gel electrophoresis. UVB-induced apoptosis was observed in 4 of 11 patients with SLE (36.3%), 3 of 8 patients with CLE (37.5%) and 2 of 6 patients (33.3%) with other collagen diseases. There was no clinical correlation between clinical photosensitivity and UV-induced apoptosis. Similarly, spontaneous apoptosis was also found in lymphocytes from patients with diseases other than SLE. No apoptosis was found in normal subjects with or without UVB irradiation (25 mJ/cm2). These data suggest that UV-induced lymphocyte apoptosis may not be specific to SLE but may be common in collagen diseases.
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PMID:In vitro spontaneous and UVB-induced lymphocyte apoptosis are not specific to SLE. 954 60

Keratinocyte apoptosis may be induced by ultraviolet-B radiation and represents a potential source of fragmented autoantigens in autoimmune diseases. This study investigates whether excessive keratinocyte apoptosis occurs in the skin lesions of cutaneous lupus (CLE) and dermatomyositis (DM) and the potential mechanisms responsible for this phenomenon. Skin biopsies have been studied from 19 patients with CLE and DM, eight with scleroderma, and five healthy controls. Apoptosis was detected by in situ end-labelling of fragmented DNA. The expression of Bcl-2, PCNA, p53, and Ki-67 proteins was studied by immunohistochemistry. In DM and CLE skin, the number of apoptotic keratinocytes was significantly increased (p=0.008) compared with normal skin. In both diseases, a large accumulation of apoptotic keratinocytes and apoptotic bodies was present in the disrupted basal zone. Unlike normal skin, a large number of keratinocytes, particularly those morphologically apoptotic, expressed p53 protein. A significant increase in the number of proliferating Ki-67 positive (p=0.0007) and PCNA-positive (p=0.0008) nuclei was also observed. In both CLE and DM, exaggerated and inappropriate keratinocyte apoptosis occurs. It is associated with increased expression of p53 and PCNA. This suggests that normal solar radiation alone or in combination with additional local factors induces DNA damage and excessive keratinocyte apoptosis in these autoimmune diseases of the skin. Apoptosis can mediate the severe epidermal lesions observed in both diseases and the release of fragmented autoantigens into the dermis.
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PMID:Keratinocyte apoptosis and p53 expression in cutaneous lupus and dermatomyositis. 1039 42

This article will review and update information about the pathogenesis, clinical presentation, diagnosis, and treatment of cutaneous lupus erythematosus. Lupus erythematosus (LE) can present as a skin eruption, with or without systemic disease. Cutaneous LE is subdivided into chronic cutaneous LE, subacute cutaneous LE and acute LE. The prevalence of systemic lupus erythematosus (SLE) is 17-48/100,000 population worldwide. Skin disease is one of the most frequent clinical complaints of patients suffering from SLE. It has been found to occur in up to 70% of patients during the course of the disease. The most frequent mucocutaneous manifestations of SLE are malar rash (40%), alopecia (24%), and oral ulcers (19%). It has been suggested that risk factors that are more likely to signal transition of cutaneous into systemic LE are high ANA titers (> 1:320) and the presence of arthralgias. CLE patients who exhibit these symptoms should be monitored closely, since they may be at increased risk to develop SLE.
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PMID:Cutaneous lupus erythematosus: a review. 1217 Aug 73

HMGB1 is a pro-inflammatory cytokine that together with TNF-alpha and IL-1beta is involved in the pathogenesis of spontaneously occurring skin lesions in lupus erythematosus. The purpose of the present study was to explore the sequence of events in HMGB1, TNF-alpha and IL-1beta expression under development and resolution of experimentally induced CLE lesions. The study involved investigation of 38 serial skin biopsies acquired from photoprovoked skin lesions of nine CLE patients, using immunohistochemical staining of tissue sections. In biopsies from the clinically most active phase of skin involvement extracellular, secreted HMGB1 and increased cytoplasmic HMGB1 were found, as compared with the late and fading lesions or non-lesional skin. Besides HMGB1, increased expression of TNF-alpha and IL-1beta was observed in dermal infiltrates of the induced CLE lesions. These cytokines were however not upregulated in all lesions, and increased expression of IL-1beta was seen predominantly in late biopsies.In conclusion, extracellular and cytoplasmic HMGB1 coincides with the clinically most active phase of photoinduced lesions of cutaneous lupus, and suggests that HMGB1 is an important factor in the inflammatory autoimmune process of CLE. HMGB1 can induce expression of TNF-alpha and IL-1beta, and formation of a pro-inflammatory loop between HMGB1, TNF-alpha, and IL-1beta may be responsible for the prolonged and sustained inflammation in CLE.
Lupus 2007
PMID:Translocation of the novel cytokine HMGB1 to the cytoplasm and extracellular space coincides with the peak of clinical activity in experimentally UV-induced lesions of cutaneous lupus erythematosus. 1789 2

Genetic differences are involved in the development of lupus erythematosus (LE). Skin lesions are influenced by environmental triggers such as ultraviolet light, temperature, and chemical stresses, and the patterns of skin lesion are variable in cutaneous LE such as systemic LE (SLE), chronic discoid LE (CDLE), subacute cutaneous LE (SCLE), and LE tumidus (LET). Although there are a few conflicting reports, many Japanese dermatologists feel there are photosensitivity differences in lupus erythematosus between Asian and Caucasian subjects with SCLE and LET. HLA studies in Japanese subjects revealed that HLA-DRB1*1501 association was with both CDLE and SLE. The association between HLA-Cw6 and CDLE was first reported in Japanese population, and a HLA-A33-B44-DRB1*1302 haplotype showed a positive association in CDLE. However, these results are not compatible with those from Caucasian subjects. There are no significant associations among HLA studies, photosensitivity, and anti-Ro/SS-A antibodies in Japanese CLE patients. Photosensitivity will be a key factor to dissolve multi-factorial complexes of LE etiopathogenesis. Our present understanding is that an axis of photosensitivity, anti-Ro/SS-A antibodies and apoptosis via TNF are the best (markers) to verify the contribution of genetics in SCLE, LET, and other CLEs. The incidence and photosensitivity of SCLE and LET are much lower in Japanese than in Caucasian subjects. However, this discrepancy may open the window for investigating CLE pathogenesis through global collaborations. For this purpose and goal, a new and more conventional method should be developed for the examination of so-called photosensitivity.
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PMID:Ethnic differences in immunogenetic features and photosensitivity of cutaneous lupus erythematosus. 1879 90

Lupus erythematosus (LE) is an autoimmune disease that can affect one or more internal organs (systemic LE [SLE]) as well as the skin (CLE). Common cutaneous subtypes of CLE are chronic CLE (CCLE) and subacute CLE (SCLE). CCLE is the only type of CLE which heals with scarring and this may affect any site in the body. The fact that inflammation in CCLE generally involves the bulge area of the follicles (where the stem cells reside) raises the possibility that damage to the stem cells may be one process leading to permanent loss of follicles. One of the most useful distinctive markers of the stem cells is cytokeratin 15 (CK15) and this has been used in some studies to demonstrate the involvement of the bulge region in the scarring process in primary cicatricial alopecia and DLE. The bulge region appears to be involved in the scarring process in CLE and other types of cicatricial alopecia as part of broader involvement of the hair follicles; it is secondarily affected by the surrounding inflammatory cell infiltrate. Expression of the stem cell marker CK15 diminished and was then absent indicating either damage to stem cells or differentiation to help in the repair process.
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PMID:Hair follicle stem cells in the pathogenesis of the scarring process in cutaneous lupus erythematosus. 1916 47

Lupus erythematosus is a chronic and inflammatory multiorgan disease with variable clinical appearance and variable course. Most patients with systemic lupus erythematosus show cutaneous manifestations and conversely, all forms of cutaneous LE may change into a systemic involvement. Specific lesions of cutaneous LE are classified in different subtypes of acute cutaneous lupus erythematosus (ACLE), subacute cutaneous lupus erythematosus (SCLE), chronic cutaneous lupus erythematosus (CDLE) and intermittent cutaneous lupus erythematosus (ICLE) according to clinical, histological and immunoserological parameters. Regular laboratory tests are important to monitor the activity and course of the disease or side effects of the therapy. In case of clinical or laboratory dysfunctions of internal organs, additional technical investigations are necessary. Histology is needed to support clinical diagnosis. A large number of drugs are able to induce SCLE, e.g. hydrochlorothiazide, terbinafine, or angiotensin-converting enzyme inhibitors. Drug-induced SCLE can be differentiated by possible complementary immunoserological parameters. Neonatal lupus can be induced by transplacental transmission of maternal anti-Ro(SS-A) and anti-La(SS-B)-antibodies. Children with neonatal lupus might suffer from congenital atrioventricular block. Their mothers may suffer from active LE, but can be clinically healthy as well. As a consequence, pregnancies at risk should be monitored in short intervals by serial echocardiographic interventions. Protection against UV light is recommended for all types of CLE. There are some topical and many systemic treatment options e.g. topical and systemic glucocorticosteroids, antimalarial drugs, dapsone, azathioprine, or mycophenolate mofetil with different response to skin or organ involvement.
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PMID:The different faces of cutaneous lupus erythematosus. 1935 21

Skin lesions of collagen diseases are influenced by environmental triggers, such as UV light, and are variable in cutaneous lupus erythematosus (LE), such as systemic LE (SLE), chronic discoid LE (CDLE), subacute cutaneous LE (SCLE), and LE tumidus (LET). Although there are a few conflicting reports on photosensitivity in collagen diseases, many Japanese dermatologists feel there are photosensitivity differences in LE between Asians and Caucasians with SCLE and LET. To address this issue, we have carried out genetic studies of Japanese SLE and CDLE patients and reviewed the race differences in photosensitivity of cutaneous LE from Japanese studies. Human leukocyte antigen (HLA) studies in Japanese patients revealed that HLA-DRB1*1501 association was with CDLE and SLE. The association between HLA-Cw6 and CDLE was first reported in a Japanese population, and a HLA-A33-B44-DRB1*1302 haplotype showed a positive association in CDLE. However, these results are not compatible with those from Caucasian subjects. There are no significant associations among HLA studies, photosensitivity, and anti-Ro/SS-A antibodies in Japanese CLE patients. Photosensitivity will be a key factor to dissolve multifactorial complexes of LE etiopathogenesis. An axis of photosensitivity, anti-Ro/SS-A antibodies, and apoptosis via tumor necrosis factor-alpha is the best marker to verify the contribution of genetics in CLE patients. The incidence and degree of photosensitivity of SCLE and LET are much lower in Japanese than in Caucasians. This discrepancy may lead to investigations of CLE pathogenesis through global collaborations.
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PMID:Race differences in immunogenetic features and photosensitivity of cutaneous lupus erythematosus from the aspect of Japanese studies. 1975 98

Background Lupus erythematosus (LE) is a chronic, autoimmune disease resulting from an interaction of genetic, environmental and hormonal factors and characterized by a spectrum of clinical forms with variable evolution from a localized cutaneous form to a life-threatening systemic form. Objective To analyse and compare the prevalence and characteristics of the main clinical and immunological manifestations of subacute cutaneous LE (SCLE) and chronic CLE (CCLE). Methods A total of 270 patients with CLE (112 patients with SCLE and 158 patients with CCLE) were studied retrospectively. The clinical and serological characteristics of all the patients were collected in a chart review. Results The patients with SCLE had a higher prevalence of annular and papulosquamous lesions, Raynaud phenomenon, mucous membrane ulcers, malar rashes, photosensitivity, vasculitis and a lower frequency of discoid lesions and alopecia compared with patients with CCLE. Patients with SCLE had a higher prevalence of arthralgias (P < 0.001), xerophthalmia (P = 0.045), arthritis (P < 0.001), nephropathy (P = 0.003) and systemic LE (SLE) (P < 0.001) compared with patients with CCLE. Patients with SCLE also had a higher frequency of laboratory and serological abnormalities than patients with CCLE. Generalized discoid LE (DLE) was associated with a higher prevalence of photosensitivity (P < 0.001), panniculitis (P = 0.009) and SLE (P = 0.003) than localized DLE. In patients with SCLE and those with CCLE, photosensitivity, arthralgias, arthritis, nephropathy and xerophthalmia were associated with SLE. In patients with SCLE, significant correlations existed between clinical and immunological data. Conclusions In our series, differences in the expression of CCLE and SCLE were found with respect to the distribution and type of lesions, systemic features and immunological findings.
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PMID:Comparative analysis of subacute cutaneous lupus erythematosus and chronic cutaneous lupus erythematosus: clinical and immunological study of 270 patients. 1978 96


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