Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with systemic lupus erythematosus (SLE) and deep fungal infection are described. Two patients had disseminated cryptococcal infection and the third disseminated histoplasmosis. Allwere receiving corticosteroids at the time fungal infection developed. One patient with disseminated cryptococcosis improved after treatment with amphotericin B and 5-fluorocytosine. The other patient with disseminated cryptococcosis died before adequate therapy could be given. The patient with histoplasmosis responded satisfactorily to amphotericin B. A survey of the literature revealed 30 additional cases of deep fungal infection in patients with SLE, most of whom were on corticosteroid therapy. The majority of the patients had candidiasis (14 patients); 11 patients had severe cryptococcal infection. Other fungal infections reported were histoplasmosis, aspergillois, coccidioidomycosis, and maduromycosis caused by Allerscheria boydii. Twenty-seven patients died; in 22 death was related to the fungal infection. The fungal infection was not diagnosed until necropsy in at least 11 persons. Deep fungal infections should be considered whenever patients with SLE have fever of unknown origin, diffuse pulmonary infiltrates, or unexplained CNS symptoms.
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PMID:Deep fungal infection in systemic lupus erythematosus - three cases reported, literature reviewed. 118 36

The incidence and prevalence of histoplasmosis in Southeast Asia has not been extensively described. The first microbiologically documented case of disseminated histoplasmosis with cutaneous papulonodules in a 56-year-old woman from the Philippines is reported. She presented with fever and generalized papulonodular lesions in various stages, which evolved into vesicles with central necrosis that resembled molluscum contagiosum with an indurated erythematous halo. Biopsies revealed a granulomatous mass of lymphohistiocytic and epithelioid cells with intracellular budding yeast cells and dark nuclei. Cultures were positive for Histoplasma capsulatum. The patient was treated with amphotericin B (3 g) and 5-fluorocytosine (50 mg/kg/day), followed by ketoconazole (400 mg/day). Her clinical course was complicated by intractable hemolytic anemia that was initially treated with corticosteroids. A splenectomy was subsequently performed. Pneumonia and a brain abscess caused by Nocardia asteroides were secondary complications. Nine months after her admission, repeat testing was diagnostic for systemic lupus erythematosus. This patient serves to re-emphasize that cutaneous lesions in an immunocompromised patient must be evaluated by biopsy and culture analysis. Disseminated histoplasmosis in the immunocompromised host may present with unusual cutaneous lesions, and must be considered even in a nonendemic area.
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PMID:Disseminated histoplasmosis with unusual cutaneous lesions in a patient from the Philippines. 137 51

A 39-year-old woman with systemic lupus erythematosus suffered a prolonged neurological illness associated with very low levels of glucose in her cerebrospinal fluid (CSF). Six months later, and after numerous CSF investigations, Histoplasma capsulatum was cultured. To our knowledge, this is the first report of cerebral histoplasmosis in Australia in a patient who is not HIV positive.
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PMID:Cerebral histoplasmosis in an Australian patient with systemic lupus erythematosus. 973 78

Histoplasma capsulatum is a pathogenic fungus endemic to North, Central, and South America. Histoplasmosis is primarily acquired by inhalation and in immunocompetent hosts infection is generally limited to the lungs. Histoplasmosis may disseminate systemically in hosts with defective cell-mediated immunity or massive inoculation. Systemic lupus erythematosus (SLE) is an autoimmune disorder associated with multiple primary and drug-related immunological defects that predispose patients to infections. Disseminated histoplasmosis has only rarely been described in association with SLE. We describe a 32-year-old woman with SLE who had a 2-year history of irregular menses and a confirmed anovulatory state, secondary to ovarian histoplasmosis. The ovarian histoplasmosis was discovered incidentally at surgery for a persistent colo-cecal fistula, which had developed 6 months earlier and was originally associated with an Actinomyces and Fusobacterium pelvic abscess. The patient had no evidence of active pulmonary histoplasmosis and her disseminated histoplasmosis likely resulted from re-activation of latent disease. This is the first description of disseminated histoplasmosis presenting as ovarian dysfunction in a patient with SLE.
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PMID:Ovarian histoplasmosis in systemic lupus erythematosus. 1084 Aug 36

Monoclonal antibodies are increasingly used to modulate immunologically mediated diseases such as rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus, Crohn's disease, multiple sclerosis and systemic vasculitis. Constructs of monoclonal antibodies to tumour necrosis factor (TNF) alpha differ with respect to their structure, effects and immunogenic side effects. Clinical experience with TNF alpha-neutralizing therapy has revealed several other side effects over the past few years. The most important is increased infection rates, especially the activation of (latent) tuberculosis, although other opportunistic infections such as listeriosis, Pneumocystis carinii pneumonia, histoplasmosis, candidiasis and aspergillosis have also been reported. Furthermore, results from clinical studies indicate that TNF alpha-neutralizing therapy should not be given to patients with cardiac failure (NYHA class III or IV) or a history of demyelinating disease. An increased incidence of malignancies has not been observed up to now, but data from the long-term follow-up are not yet available.
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PMID:[The treatment of chronic inflammatory diseases with monoclonal antibodies against tumor necrosis factor: side effects, contraindications and precautions]. 1235 84

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

This report describes the coexistence of three patients with rheumatic diseases (systemic lupus erythematosus, rheumatoid arthritis, and dermatomyositis) and infections because of Histoplasma capsulatum. Connective tissue diseases and histoplasmosis share several clinical findings. Therefore, histoplasmosis could be misdiagnosed as connective tissue disease or a flare of these diseases. Such cases highlight the importance of awareness of histoplasmosis in immunocompromised patients, particularly in those originating from endemic areas.
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PMID:Unusual manifestation of histoplasmosis in connective tissue diseases. 1754 96

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

Progressive disseminated histoplasmosis is a disease where Histoplasma capsulatum affects multiple organs due to the inability of host cellular immunity to control the infection. Progressive disseminated histoplasmosis mainly involves the bone marrow, liver, and lungs. We report an unusual initial presentation of progressive disseminated histoplasmosis presenting as acute tenosynovitis in a systemic lupus erythematosus (SLE) patient. This report highlights the point that H. capsulatum may present as focal lesions and a high level of suspicion is needed to make the diagnosis, especially in SLE patients. We specifically reviewed reported cases of progressive disseminated histoplasmosis in SLE patients, and a review of the literature is presented.
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PMID:Progressive disseminated histoplasmosis in systemic lupus erythematosus-an unusual presentation of acute tenosynovitis and a literature review. 2306 46

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


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