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)

Specimens representing 17 cases of each of oral mucosal lupus erythematosus (LE) and lichen planus were examined under the light microscope to establish a set of histopathologic criteria that would distinguish between the two. Statistical analysis showed that significant differences in histopathology exist between the two diseases. A classic case of LE was found to exhibit the following characteristics: vacuolization of keratinocytes, patchy PAS-positive deposits subepithelially, edema in the lamina propria, PAS-positive thickening of blood vessel walls, and the presence of a severe or perivascular inflammatory cell infiltrate. A number of other less significant alterations were also identified. It is concluded from this study that oral LE in most cases is characteristic enough to provide a definitive diagnosis at the light microscopic level.
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PMID:A histopathologic study of oral mucosal lupus erythematosus. 271 52

The case of a 48-year-old patient with systemic lupus erythematosus is discussed. Under immunosuppressive therapy, symptomless papules occurred on the shoulders, back, chest and face. Histologically, there were deposits of mucinous matter which produced an intensive blue colour in the HALE-PAS and alcian blue colour test. The epidermal and dermal inflammatory changes which typically occur with lupus erythematosus were absent. Whereas mucin is commonly diagnosed in lupus erythematosus, the clinical manifestation of papulous mucinosis is a rare but diagnostically significant phenomenon, since it can occur without further findings which are typical of lupus erythematosus.
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PMID:[Papular mucinosis. A rare cutaneous manifestation of lupus erythematosus]. 796 Jul 74

We have previously shown that murine IgG3 monoclonal autoantibodies with cryoglobulin activity, derived from lupus-prone mice, are able to induce glomerular lesions resembling the "wire-loop" lesion typically described for human lupus nephritis. In the present study, we have further assessed the nephritogenic potential of four IgG3 anti-hapten, trinitrophenyl (TNP), monoclonal antibodies (mAb) obtained from non-autoimmune mice immunized with TNP-conjugated foreign antigens. Our results showed that two of four IgG3 anti-TNP monoclonal cryoglobulins were capable of inducing glomerular lesions, characterized by voluminous intracapillary thrombi and mesangial deposition of PAS-positive materials, which differed from "wire-loop" lesions generated by IgG3 monoclonal cryoglobulins with autoantibody activities. These anti-TNP monoclonal cryoglobulins, however, failed to induce glomerular lesions when mice were kept at 37 degrees C after the mAb administration. This finding formally proves that the cryoglobulin activity is critically involved in the development of glomerular lesions induced by IgG3 anti-TNP mAb. In addition, we have demonstrated a remarkable difference in the nephritogenic activities of two IgG3 anti-TNP mAb, which exhibit a marked sequence homology in the variable regions of their heavy and light chains (91.5% and 99.1% at the amino acid level, respectively) and an identical isoelectric point. Our results indicate first, that IgG3 monoclonal cryoglobulins are able to generate two different kinds of glomerular lesions, and second, that a subtle difference in variable region sequences may determine not only the nephritogenic activities, but also the type of glomerular lesions mediated by IgG3 cryoglobulins.
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PMID:Glomerulopathy induced by IgG3 anti-trinitrophenyl monoclonal cryoglobulins derived from non-autoimmune mice. 800 99

Four cases of Hypertrophic Lupus Erythematosus (HLE) were reported. The lesions of HLE were observed on the forearms, face and hands in all four cases. Clinically, the lesions were erythematous, hyperkeratotic plaques. The clinical course was marked by chronicity and progression of the lesion. Histologically, marked hyperkeratosis, parakeratosis, acanthosis, degenerative changes of basal cells in H/E stain, and thickened, multilayered basement membrane in PAS stain, were observed. The observations of Dylon stain revealed that localized amyloid deposition was observed in all four cases of HLE lesions, as fluorescent-orange colored amyloid deposits in the papillary dermis and subepidermal areas at near orjust below the dermo-epidermal junction appeared under fluorescent microscope. On the basis of clinical and histological observations, we suggest that chronic irritation, such as sunlight exposure over a long-duration, might have caused the characteristic abnormalities at the dermo-epidermal junction and also initiated the frequency of amyloid deposits locally secondary to the diseases. We compared our HLE cases to other types of lupus erythematosus (LE) skin lesions, as to whether deposition of amyloid materials were frequently observed or not. Amyloid deposition was observed in one case of DLE and none of the SLE cases. Localized amyloid deposition was more frequently observed in skin lesions, secondary to HLE disease, as compared to other types of LE.
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PMID:Amyloid deposition is frequently observed in skin lesions of hypertrophic lupus erythematosus. 1243 94

Utilizing the fluorescent antibody method for the histologic demonstration of localized gamma-globulins, we have made the following observations (in contradistinction to the lack of such findings in a variety of normal and pathologic, control kidneys). In systemic lupus erythematosus (a) gamma-globulins were localized in the thickened capillary walls, the "wire-loop" lesions, and the so called "hyaline thrombi" in glomeruli; (b) these sites of localization of gamma-globulins were correlated to a considerable degree with the pattern of accentuated eosinophilia of the glomeruli, as seen in hematoxylin-eosin sections, or with the pattern of PAS-positive areas in the glomeruli in sections stained with the periodic acid-Schiff reaction; (c) and gamma-globulins were localized rarely in large cytoplasmic granules in tubular epithelium and occasionally in glomerular capsular crescents, tubular protein casts, and inflammatory cells, particularly in the cytoplasm of cells identified as immature and mature plasma cells. In nephrotic glomerulonephritis (a) gamma-globulins were localized in the glomerular basement membrane and appertaining structures in chronic membranous glomerulonephritis; (b) gamma-globulins were apparently localized in the altered mesangium in chronic lobular glomerulonephritis; and (c) in the tubular protein casts, presumably representing abnormal glomerular filtrates, gamma-globulins were present in a lesser concentration and other serum proteins in a greater concentration than found in the glomeruli. In positive lupus erythematosus preparations the nuclei of leukocytes, while undergoing transformation and subsequent phagocytosis to form lupus erythematosus cells, were the sites of localization of gamma-globulin (presumably the lupus erythematosus factor) whereas in control preparations no nuclear localization of gamma-globulin occurred. These observations are discussed in relation to the pathogenesis of renal lesions in systemic lupus erythematosus, chronic membranous glomerulonephritis, and amyloidosis.
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PMID:Role of gamma globulins in pathogenesis of renal lesions in systemic lupus erythematosus and chronic membranous glomerulonephritis, with an observation on the lupus erythematosus cell reaction. 1344 31

This study, based upon 528 laboratory examinations and 16 complete autopsies of NZB/Bl mice, deals with autoimmune manifestations (as shown by hypergammaglobulinemia, Coombs positive hemolytic anemia, and the occasional presence of lupus- and rheumatoid-like factors) and mainly with the pathology and the pathogenesis of glomerulonephritis in these mice, a model system of membranous glomerulonephritis with spontaneous and insidious onset, progression through chronic stages, and almost certainly induced by immunological, and autoimmune, mechanisms. The earliest and lasting histological change was hyaline thickening of the capillary walls and adjacent intercapillary regions of the glomerular tufts, corresponding in location to polysaccharide-rich capillary basement membrane and mesangial materials. Distributed focally and diffusely in the glomerular tuft and eventually sparing no glomerulus, hyaline, granular, and fibrillar ("spongy fiber") materials produced narrowing of capillary lumens by concentric or eccentric encroachment upon them. In the later stages hyaline lobulation and sclerosis of the glomerular tufts occurred. Thus the lesions corresponded to those seen in human focal and diffuse membranous, chronic lobular, and lastly (intracapillary) sclerosing glomerulonephritis. In all instances of glomerulonephritis the glomerular tufts contained selective localizations of mouse immunoglobulins corresponding in distribution to that of the hyaline and (PAS-positive) polysaccharide-rich materials in the focal and diffuse membranous and lobular lesions and in amounts increasing with the severity of glomerular disease. The mouse immunoglobulins were extracted from frozen sections of glomerulonephritic kidneys and were then capable of recombination with glomerular tufts in sections of autologous or isologous glomerulonephritic kidneys from which in vivo localized immunoglobulins had been extracted. The pattern of recombination with glomerular tufts was similar to that of in invo localized immunoglobulins. The extracted immunoglobulins did not show affinity for mouse red cells (in the indirect Coombs test) nor for autologous or isologous cell nuclei (in the immunofluorescence test). The serum of mice with severe glomerulonephritis contained immunoglobulins with in vitro affinity for extracted autologous or isologous glomerular tufts. Thus circulating as well as localized antibodies were demonstrated. The immunogenic materials (autoantigens) may have been formed in the glomerular tufts or accumulated in them from some other source, such as the circulating plasma; however they corresponded in location to polysaccharide-rich capillary basement membrane and mesangial materials. The spleen was identified at the cellular level as the main site of formation of autoantibodies to red cells, as well as the main site of red cell destruction. Some evidence was brought forth suggesting that these autoantibodies were "heavy" or gammaM-globulins. More studies are in progress.
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PMID:AUTOIMMUNE DISEASE IN NZB/BL MICE. I. PATHOLOGY AND PATHOGENESIS OF A MODEL SYSTEM OF SPONTANEOUS GLOMERULONEPHRITIS. 1432 72

Allogeneic mixed chimerism achieved by low-dose total body irradiation (TBI) and anti-CD40L monoclonal antibody (mAb) with donor bone marrow transplantation (BMT) and host T cell depletion overcomes both allo- and autoimmunity. We investigated whether a similar regimen without T cell depletion cured diffuse proliferative glomerulonephritis. Male BXSB mice (H-2b) were injected with 20 x 10(6) BALB/c (H-2d) BM cells. When indicated, 3 Gy TBI on day -1 and anti-CD40LmAb (2 mg) on day 0 of BMT was given. Skin grafting was performed 1 day after BMT. BXSB mice were divided into four groups--I: BMT with TBI and anti-CD40LmAb; II: TBI; III: TBI and anti-CD40LmAb; and IV: no treatment. Chimerism in peripheral blood was analyzed. The kidney was examined histologically. TBI with anti-CD40LmAb and BMT allowed induction of multilineage mixed chimerism and donor-specific tolerance to skin grafts without graft-versus-host disease (GVHD). There was significant decrease in glomerular PAS-positive material deposition score, glomerular cell numbers, IgG, and C3 deposition in chimeric mice. All chimeric mice survived. Allogeneic mixed chimerism induced by a less toxic, nonlymphoablative regimen achieved allograft tolerance and cured glomerulonephritis in BXSB lupus mice.
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PMID:Allogenic mixed chimerism induced by nonlymphoablative regimen including donor BMT with low-dose TBI and anti-CD40L cured proliferative glomerulonephritis in lupus mice. 1791 51

Coccidioidomycosis is usually acquired by inhalation of spores of Coccidioides immitis and C. posadasii. The disease ranges from a self-limited acute pneumonia (Valley Fever) to a disseminated disease. We present a 44-year-old healthy male who had patchy hair loss of several months duration resembling discoid lupus. He developed a firm non-scaly red plaque on the right forehead. Initial biopsy showed spongiotic dermatitis, and he was treated with systemic steroids. He then developed forehead and periorbital cellulitis and was treated with systemic antibiotics. A second biopsy showed fungal hyphae, and he was treated with itraconazole 200mg bid for 4months beyond clinical resolution. A year later, he presented with intermittent swelling of the right forehead lesion and worsening of the scalp lesions. A forehead biopsy showed interface dermatitis and negative PAS stain for fungi. Scalp biopsy was highly suggestive of discoid lupus and he was started on plaquenil. Many months later, a third biopsy showed fungal infection, and the culture grew C. immitis. He was treated with itraconazole. Retrospectively, the patient gave a history of Valley fever 6 years back when he was in Arizona, USA.
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PMID:Recurrence of cutaneous coccidioidomycosis 6 years after valley fever: A case presentation and literature review. 2881 Nov 15

Cutaneous lupus erythematosus (CLE) is a chronic-relapsing disease. It is defined as a LE localized to the skin without any significant systemic symptoms. Its annual incidence is of 4 cases per 100,000 persons with a prevalence of 73 cases per 100,000 persons. The etiology is unknown but it is considered as a prototype of autoimmune disease in which genetic factors (HLA), environmental factors (photo exposure and cigarette smoking) and pharmacological agents play an important role. The most accepted classification includes three clinical variants: acute (ACLE), subacute (SCLE) and chronic (CCLE). A fourth variety is the intermittent form (ICLE) also called "lupus tumidus" (LET) which is considered by some authors a distinct form from CCLE. The skin lesions are subdivided into LE specific and LE non-specific. The latter have a considerable importance as a symptom of evolution of the disease towards a systemic form of lupus (SLE). The histopathology of CLE is characterized by an interface dermatitis with vacuolization of the basal layer, a predominantly lymphocytic, perivascular and periadnexal infiltrate, epidermal and follicular hyperkeratosis, deposit of positive PAS material at the dermo-epidermal junction leading to atrophic-cicatricial evolution. Depending on the clinical variants, these microscopic features are more or less evident and are associated with peculiarities such as deposits of mucin (SCLE and LET), involvement of the panniculus in LE panniculitis, disappearance of the adnexa (cicatricial alopecia). The relationship between SLE/CLE is still under study: the progression of CLE in SLE is reported in a variable percentage of cases ranging from 12 to 18%. CLE therapy is aimed at preventing recurrences and scarring outcomes. Photoprotection with clothing, chemical and physical sunscreens active on UVA and UVB radiations is very important. Topical therapy is based on the use of steroids and calcineurin inhibitors, while the systemic therapy includes hydroxychloroquine as the first drug of choice.
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PMID:Cutaneous lupus erythematosus: clinico-pathologic correlation. 2936 45