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 origin of gingival inflammation is occasionally different from that of routine plaque-associated gingivitis, and such non-plaque-associated types of gingivitis often present characteristic clinical features. Examples of such forms of gingivitis are specific bacterial, viral, and fungal infections. Specific bacterial infections of gingiva may be due to Neisseria gonorrhea, Treponema pallidum, streptococci, and other organisms. The most important viral infections of gingiva are herpes simplex virus type 1 and 2 and varicella-zoster virus. Fungal infections may be caused by several fungi, the most important of these being Candida species including C. albicans, C. glabrata, C. krusei, C. tropicalis, C. parapsilosis, and C. guillermondii. Gingival histoplasmosis is a granulomatous disease caused by the fungus Histoplasma capsulatum and, as for the other specific infections of gingiva, a confirmed diagnosis may require histopathologic examination and/or culture. Atypical gingivitis may also occur as gingival manifestations of dermatological diseases, the most relevant of these being lichen planus, pemphigoid, pemphigus vulgaris, erythema multiforme, and lupus erythematosus. Non-plaque induced gingival inflammation can be caused by allergic reactions to dental restorative materials, toothpastes, mouthwashes, and foods. In addition, gingival inflammation may result from toxic reactions, foreign body reactions, or mechanical and thermal trauma.
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PMID:Non-plaque-induced gingival lesions. 1086 72

We studied the clinical and immunological effects of Rituximab (anti-CD20) therapy in patients with lupus nephritis. In an open clinical trial, 22 patients with active systemic lupus erythematosis and renal involvement (mainly class III and IV according to the WHO classification) that was refractory to conventional therapy were studied. In all these patients, Rituximab (0.5 to 1.0 g at days 1 and 15) was added to the immunosuppressive therapy and its therapeutic effect was evaluated. In addition, the levels and function of regulatory T lymphocytes and the apoptosis of immune cells were assessed. We found a significant reduction in disease activity (p < 0.05, MEX-SLEDAI index), and proteinuria (p < 0.05) at days 60 and 90 of Rituximab therapy. Although most patients showed improvement in creatinine clearance and erythrocyturia, no significant changes in these parameters were detected. In most patients (20/22), B cell depletion was observed, but no clear-cut effect of Rituximab on complement levels or auto-antibody titers was detected (p > 0.05 in all cases). One patient died at day 70 with invasive histoplasmosis. No important adverse effects of Rituximab therapy were registered in other patients. A significant enhancement in the levels of different CD4+ regulatory cells (TREG, Th3, Tr1), but not CD8+ Ts lymphocytes, was observed at day 30. This increase was sustained for TREG cells at day 90, and accompanied by an improvement in their regulatory function. In addition, we observed an unexpected increase in the apoptosis of T cells at day 30. Interestingly, the enhancement in the suppressive function of TREG cells was not observed in the two patients that showed the poorest clinical response to Rituximab. We conclude that the data obtained in this open clinical trial suggest that Rituximab is a promising candidate for randomized controlled trials in patients with lupus nephritis refractory to the conventional immunosuppressive therapy. The effects of Rituximab on regulatory cells and apoptosis of T lymphocytes are interesting and its possible role in the putative effect of this biological agent in systemic lupus erythematosis deserves additional studies.
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PMID:Clinical and immunological effects of Rituximab in patients with lupus nephritis refractory to conventional therapy: a pilot study. 1667 95

Through its anatomical, topographical, and functional distinctiveness, more than all other parts of the body, the hand is the interface between humans and their environment. All types of stimulus produce cutaneous signs in the hands, notably cold, light, pressure, contact, etc. Exposure to light makes it the region where photodermatosis is expressed, but also a particular site for cutaneous carcinogenesis. The countless chemical substances that the hand encounters can create specific or particular diseases in this location (irritative dermitis, contact eczema, hyperkeratosis, atrophy, etc.). The hand is also the site of infectious dermatosis transmission (erysipeloid, orf, mycobacteriosis, etc.), sometimes exotic (chromomycosis, histoplasmosis), and the site of plant penetration (protothecosis or more commonly thorns and splinters). The complexity of its vascularization and its many bones, joints, and tendons explain why it is a preferred area for signs of systemic diseases (diverse forms of lupus, dermatomyositis, inflammatory rheumatism, etc.). The nail unit alone shows innumerable signs of exogenic diseases, but also reflects certain internal diseases localized here with often characteristic signs. Here more than anywhere else, dermatology opens out to all of medicine.
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PMID:[Hand for the dermatologist]. 2118 84

Histoplasmosis is a multifaceted condition caused by the dimorphic fungi Histoplasma capsulatum whose infective spores are inhaled and reach the lungs, the primary organ of infection. The meningeal form, considered one of the most serious manifestations of this mycosis, is usually seen in individuals with impaired cellular immunity such as patients with acquired immunodeficiency syndrome, systemic lupus erythematous or solid organ transplantation, and infants given their immunological immaturity. The most common presentation is self-limited and occurs in immunocompetent individuals who have been exposed to high concentrations of conidia and mycelia fragments of the fungi. In those people, the condition is manifested by pulmonary disorders and late dissemination to other organs and systems. We report a case of central nervous system histoplasmosis in an immunocompetent child.
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PMID:[Histoplasmosis of the central nervous system in an immunocompetent patient]. 2550 38

The authors present four cases of Wegener's granulomatosis patients with multiorganic manifestation forms, but with a prevalent involvement in upper-airway. Granulomatosis diseases of the nose include bacterial infections (rhinoscleroma, tuberculosis, syphilis, lupus, and leprosy), fungal infections (rhinosporidiosis, aspergillosis, mucormycosis, candidosis, histoplasmosis, and blastomycosis) and diseases with unspecified etiology (Wegener's granulomatosis, mediofacial malignant granuloma, and sarcoidosis). We consider an interesting experience regarding Wegener's granulomatosis due to its rarity, being an autoimmune systemic disease, with continuous evolution and multiorganic involvement. The beginning of the disease is like upper airway affection, a kind of "persistent cold", being difficult to differentiate it from a common cold in the head, with a prolonged evolution. It is important to mention that we establish the diagnosis of Wegener's granulomatosis starting with Ear Nose and Throat (ENT) clinical exam, followed by other tests and investigations realized in our Clinic and completed with specialty tests (nephrology, internal medicine and dermatology), meaning that we need a close cooperation with these medical specialties. All the patients presented multiorganic involvement. Notably significant for our four cases is the prolonged evolution in a stable condition in one patient.
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PMID:The involvement of upper airway in Wegener's granulomatosis - about four cases. 2619 39

We developed and analyzed an Enzyme-Linked Immunosorbent Assay (ELISA) in order to detect antibodies in sera from sporotrichosis patients. We used a crude antigen of Sporothrix schenckii sensu stricto, obtained from the mycelial phase of the fungi. Positive sera were analyzed by other serological techniques such as double immunodiffusion (IGG) and counterimmunoelectrophoresis (CIE). The assay was validated by using sera from patients with other pathologies such as: histoplasmosis, paracoccidioidomycosis, tuberculosis, leishmaniasis, lupus and healthy individuals as negative controls. For the Sporothrix schenckii sensu stricto antigen, we found a 100% of specificity by every technique and sensitivity higher than 98% with IDD, CIE and ELISA. Our results show a high sensitivity and specificity for the Sporothrix schenckii sensu stricto antigen, so it can be used for IDD, CIE and ELISA. The results suggest that this antigen could be used in conjunction with other conventional tests for differential diagnosis and may be useful for monitoring the disease progression and response to treatment.
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PMID:[Serological diagnosis of sporotrichosis using an antigen of Sporothrix schenckii sensu stricto mycelium]. 2629 53

Histoplasmosis is a systemic fungal infection caused by dimorphic fungus, Histoplasma capsulatum. Immunocompetent individuals usually have self-limiting or localized disease whereas immunocompromised individuals develop disseminated disease. The occurrence of progressive disseminated histoplasmosis in juvenile systemic lupus erythematosus is extremely rare with only one reported case in literature showing such association. Therefore, we report a case of severe opportunistic fungal infection caused by Histoplasma in a 13-year-old girl who was diagnosed with juvenile lupus erythematosus, subsequently developed septic shock and died of the disease despite of aggressive antifungal therapy.
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PMID:A Rare Case of Juvenile Systemic Lupus Erythematosus with Disseminated Histoplasmosis. 2790 4

Granulomas of the skin may be classified in several ways. They are either infectious or non-infectious in character, and they contain areas of necrobiosis or necrosis, or not. Responsible infectious agents may be mycobacterial, fungal, treponemal, or parasitic organisms, and each case of granulomatous dermatitis should be assessed histochemically for those microbes. In the non-infectious group, examples of necrobiotic or necrotizing granulomas include granuloma annulare; necrobiosis lipoidica; rheumatoid nodule; and lupus miliaris disseminates faciei. Non-necrobiotic/necrotizing and non-infectious lesions are exemplified by sarcoidosis; foreign-body reactions; Melkersson-Rosenthal syndrome; Blau syndrome; elastolytic granuloma; lichenoid and granulomatous dermatitis; interstitial granulomatous dermatitis; cutaneous involvement by Crohn disease; granulomatous rosacea; and granulomatous pigmented purpura. Histiocytic dermatitides that do not feature granuloma formation are peculiar reactions to infection, such as cutaneous malakoplakia; leishmaniasis; histoplasmosis; lepromatous leprosy; rhinoscleroma; lymphogranuloma venereum; and granuloma inguinale.
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PMID:Granulomatous & histiocytic dermatitides. 2809 63