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

There has been a controversy as to the origin of lupus miliaris disseminatus faciei (LMDF). It was originally thought to be associated with tuberculosis, due to its histopathological similarity. Recently, this association has been doubted, although there remain reported cases of LMDF associated with Mycobacterium tuberculosis. Three patients with the clinical and histopathological features of LMDF are described. Skin from these patients was analysed by polymerase chain reaction (PCR) using two different oligoprimers for the detection of 123 bp and 165 bp DNA fragments specific for M. tuberculosis complex. With these two PCR systems, no M. tuberculosis DNA was detected in any of the LMDF patients. It was present in all positive controls and absent in all negative controls. In this study we could not demonstrate an association between LMDF and tuberculosis.
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PMID:Lupus miliaris disseminatus faciei--the DNA of Mycobacterium tuberculosis is not detectable in active lesions by polymerase chain reaction. 939 Mar 42

For 5 years, an 83-year-old man had been suffering from slightly itchy erythematous plaques with clearcut margins, located on his left thigh and on his right arm; in addition, on his right auricle there was an erythematous patch with yellowish shadings that had appeared about 3 years before and had progressively spread to the temporal-zygomatic region, the chin and the mandibular arch. These lesions were strongly suggestive of lupus vulgaris; however the conventional bacteriological examinations performed on the biopsy specimen from lesional skin were negative. A diagnosis of lupus vulgaris was achieved through the detection of the 16S rRNA gene of Mycobacterium tuberculosis in a skin biopsy of the patient by means of a polymerase chain reaction followed by a reverse cross blot hybridization, a method which allows the identification of different mycobacterial species in a single hybridization procedure.
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PMID:Polymerase chain reaction and reverse cross blot hybridization assay for detection of mycobacterial DNA in lupus vulgaris. 940 86

Both experimental and clinical forms of chronic GVHD have unique immunological features. The affected animals/individuals suffer from autoimmune disorders such as systemic lupus erythematosus (SLE), and yet they are unable to mount a self MHC-restricted T cell response to foreign antigens. Pathogenesis of the latter phenomenon was investigated in an experimental model of chronic GVHD. Chronic GVHD was induced in 8-10-week-old (B6xC3H)F1 mice by tail vein injection of 5 x 10(7) spleen cells of C3H parental strain. The recipients, when tested 3 months later, were unable to mount a T helper (Th) cell response to a randomly selected immunogen, a vaccine of l0(8) killed Mycobacterium vaccae. The animals showed evidence of generalized lymphoid hyperplasia, as indicated by GVH index >1.34, and also revealed autoantibodies against erythrocytes and dsDNA, indicating establishment of chronic GVHD. However, mice with chronic GVHD of only 3 weeks duration were able to mount the Th cell response to M. vaccae. Three consecutive immunizations of these mice at 1-week intervals, with the same immunogen, resulted in the mice becoming non-responsive to the antigen. All the three responses tested, namely the DTH, lymphoproliferation and the antibody responses, were adversely affected. The non-responsiveness induced was antigen-specific. Mice receiving two immunizations with M. vaccae responded normally to Salmonella enteritidis. Pulse treatment with cyclosporin A 0.5 mg/mouse by the i.p. route, on days 0, 1, 2, 3 and 4 at the time of immunization with M. vaccae on day 1, prevented emergence of non-responsiveness. Based on this evidence, it was concluded that repeated activation of T cells of mice with chronic GVHD induces non-responsiveness. Extent of clonal loss due to activation-induced cell death (AICD) caused by i.p. injection with a superantigen Staphylococcal enterotoxin B (SEB) was investigated in F1 mice with chronic GVHD. I.p. injection of 25 microg/mouse of SEB induced loss of SEB responding clones in both normal F1 mice and those having chronic GVHD; however, the extent of loss was much greater in the latter. In vitro antigen-specific proliferation of primed splenic T cells of normal F1 mice was observed to be quite poor when antigen was presented by APC of mice with chronic GVHD of 3 weeks duration. Proliferation profiles of T cells of normal F1 mice, in response to stimulation with concanavalin A (Con A) or SEB, were studied, using as APC irradiated spleen cells of normal F1 mice or of F1 mice with chronic GVHD of 3 weeks duration. With Con A and APC of normal F1 mice, peak proliferation was observed at 48 h, which remained at the same level up to 72 h and declined thereafter, possibly due to AICD. With SEB and the normal APC, proliferation progressively peaked at 72 h and declined thereafter. With APC of mice with chronic GVHD, the 48 h proliferative responses of both Con A and SEB were comparable to those caused by APC of normal F1 mice; however, thereafter the responses declined steeply, suggesting greater AICD. Based on these results, it was concluded that APC of mice with chronic GVHD are functionally altered to induce greater AICD.
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PMID:Antigen-presenting cells (APC) of mice with chronic graft-versus-host disease (GVHD) cause excessive activation-induced death of T helper cells. 940 51

Infection with marine bacteria is uncommon. A patient with systemic lupus erythematosus who developed concurrent infection with Shewanella putrefaciens and Mycobacterium marinum (M. marinum) is described. After bathing leg ulcers in sea water, severe cellulitis of the left leg with necrotic areas and extensive bullae developed. Infection due to S. putrefaciens was confirmed and a long course of hospitalization, oral ciprofloxacin and skin grafting was required. During hospitalization subcutaneous nodules developed on the other leg. Biopsy revealed acid-fast bacilli and culture grew M. marinum. These lesions responded to rifampicin and cotrimoxazole. Patients with leg ulcers, peripheral vascular disease, diabetes, or receiving immunosuppressive drugs may acquire unusual infections after salt water exposure.
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PMID:Concurrent infection due to Shewanella putrefaciens and Mycobacterium marinum acquired at the beach. 961 78

A single dose of pasteurized Mycobacterium bovis administered intravenously to prediabetic non-obese diabetic (NOD) mice prevented the onset of type 1 diabetes but precipitated a systemic 'autoimmune rheumatic disease' (ARD) similar to systemic lupus erythematosus. This syndrome was characterized by haemolytic anaemia, anti-dsDNA and anti-Smith antigen (Sm) antinuclear autoantibodies, increased severity of sialadenitis and glomerular immune complex deposition. Here, we examine the specificity of the autoantibody responses in M. bovis-treated NOD mice. Large amounts of antibody were detected to the Sm/ribonucleoprotein (RNP) complex, of which the 28 000 MW polypeptide appeared to be immunodominant. The IgG subclass involved in the anti-Sm response was primarily IgG2a. Antibodies against dsDNA were also detected, but the subclass of this response was mixed, with IgG2a and IgG2b being present in equal amounts. Together, these findings argue against a role for immune deviation towards T helper type 2 (Th2) responses in pathogenesis of the disease. The anti-dsDNA and anti-Sm reactivities were not mediated by polyreactive antibodies since neither antigen could cross-compete plasma antibody binding to the other in competitive enzyme-linked immunosorbent assay. The role of polyclonal B-cell activation was examined by measuring total gamma-globulin as well as IgG reactive with other nuclear antigens including Ro60, Ro52 and La, which although not a major component of the autoantibody responses in these mice, did show small but significant increases following immunization with M. bovis. Thus polyclonal stimulation, while likely to be occurring, was not directly responsible for production of anti-Sm antibodies.
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PMID:Characterization and specificity of B-cell responses in lupus induced by Mycobacterium bovis in NOD/Lt mice. 976 51

The heat-shock response of Streptococcus pyogenes following exposure to elevated growth temperatures, and the immunological reactivity of heat-shock proteins (HSPs) in streptococcal infections were studied. Two major proteins of 65 and 75 kDa were expressed when a S. pyogenes strain was shifted from 37 degrees C to heat-shock temperatures of 40, 42 and 45 degrees C. Such proteins are members of the GroEL and DnaK families recognised in a Western blot assay with polyclonal antibodies against Escherichia coli GroEL and E. coli DnaK, respectively. Two-dimensional autoradiograms of polypeptides labelled at 37 or 42 degrees C showed an increased intensity of three spots at 42 degrees C. A monoclonal antibody (MAb) against HSP 63 of Bordetella pertussis also recognised the 65-kDa inducible protein, although MAbs against Mycobacterium tuberculosis HSP 65 failed to recognise this protein. Immunoblot analysis of sera from individuals with rheumatic fever or uncomplicated streptococcal diseases revealed seven major immunogenic protein bands, two of which also reacted with anti-E. coli GroEL and DnaK polyclonal antibodies. Furthermore, antibodies to the GroEL and DnaK proteins were also detected in sera from patients with either rheumatoid arthritis or systemic lupus erythematosus. These results demonstrated a heat-shock response of S. pyogenes, and indicated the presence of an immune response against HSPs in streptococcal diseases.
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PMID:Expression of heat-shock proteins in Streptococcus pyogenes and their immunoreactivity with sera from patients with streptococcal diseases. 987 92

Mycobacterium kansasii infections of the skin have been described in 31 previously published cases. The median age of these patients is 43 years, and male patients are more frequently affected than female patients. Most patients (72%) with this infection have some alteration of their immune status, but disseminated infection is relatively uncommon (22%). We present the first reported case of cutaneous M. kansasii infection in a patient with previously diagnosed systemic lupus erythematosus. The clinical presentation is similar to that expected in lupus profundus. While the duration of treatment is long (18 months), this case demonstrates that rifampin combined with at least 2 other antibiotics can provide excellent results. Clarithromycin has demonstrated encouraging in vitro results against M. kansasii but has not yet been reported for treatment of cutaneous infections.
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PMID:Cutaneous Mycobacterium kansasii infection in a patient with systemic lupus erythematosus: case report and review. 1002 69

Intracranial tuberculomas manifesting radiologically as typical dural-based "meningiomas" have been reported, most frequently in immunosuppressed patients. Their incidence is high in developing countries; they are only sporadically observed in Western Europe and North America, usually in patients with acquired immunodeficiency syndrome (AIDS). According to published reports, intracranial tuberculomas are always due to infection by Mycobacterium tuberculosis. We report a case of a 50-year-old woman with systemic lupus erythematosus (SLE) who presented with a dural based, meningioma-like mass in the right frontal region, resulting from a localized infection by Mycobacterium avium complex. Histologically, the mass resembled a meningioma in being composed of spindly cells arranged in a fascicular pattern. Immunohistochemical stains showed this tumor to consist of a large aggregate of AFB-laden histiocytes without caseating necrosis or multinucleated giant cells.
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PMID:A meningioma-mimicking tumor caused by Mycobacterium avium complex in an immunocompromised patient. 1063 98

For a definitive diagnosis of cutaneous tuberculosis the demonstration of mycobacteria is essential, but this is generally not possible in skin lesions. Routinely available techniques have poor sensitivity and are time consuming, therefore, delaying the institution of timely therapy. The high sensitivity and speed of polymerase chain reaction (PCR) for the detection of infectious agents has prompted investigators to use this technique for the detection of Mycobacterium tuberculosis in body fluids such as cerebrospinal fluid or pleural fluid. In the present study, PCR was used to examine punch biopsy specimens from the affected skin of 10 patients with clinical diagnoses of tuberculosis verrucosa cutis, lupus vulgaris, scrofuloderma, papulonecrotic tuberculide and erythema induratum. A control group of 20 patients included individuals having skin manifestations with definite clinical diagnoses other than cutaneous tuberculosis, such as leprosy, fungal mycetoma, chronic bullous disease of childhood and pemphigus vulgaris. The PCR amplified products were dot hybridized with a probe which was random prime labelled with 32P. The results were compared with routine microbiological and histological findings. Among the test group, six of 10 (60%) were positive for M. tuberculosis by PCR, although their histopathology showed non-specific chronic inflammation with no definite diagnosis. Microbiological investigations, including acid-fast bacillus smear and culture, were positive in a single case of scrofuloderma. All patients in the control group were negative by PCR for M. tuberculosis. The data indicate that the combination of dot hybridization with PCR markedly increased the sensitivity and specificity of PCR. This may be a useful tool in the diagnosis of tuberculosis when conventional methods fail.
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PMID:Development of a polymerase chain reaction dot-blotting system for detecting cutaneous tuberculosis. 1065 97

The incidence of tuberculosis and extrapulmonary forms of this disease is increasing all over the world. Lupus vulgaris is the most prevalent form of cutaneous tuberculosis in Europe and the Middle East. Papulonecrotic tuberculid, the most common form of hyperergic response to mycobacteria or their fragments, is uncommon in children. We report lupus vulgaris with papulonecrotic tuberculid in a 12-year-old girl who had a 3-year history of slowly growing plaques on her trunk, extremities, and the tip of her nose and papuloulcerative lesions over her entire body. A skin biopsy specimen showed minimally caseating granulomatous inflammation. Staining for acid-fast bacilli was negative in both plaques and papules. Polymerase chain reaction identified Mycobacterium tuberculosis DNA in the patient's sputum, gastric fluid, and plaques and was negative in the papules. She was started on antituberculous therapy with four drugs and her lesions responded rapidly.
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PMID:Disseminated lupus vulgaris and papulonecrotic tuberculid: case report. 1079 4


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