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)

We encountered a 13-year-old boy with SLE who showed specific pathophysiology. The affected child was hospitalized because of long-standing cutaneous empyesis considered to be Staphylococcus aureus infection, followed by manifestation of meningoencephalitis-like symptoms. On a close check up, the patient was diagnosed as having SLE complicated with interstitial lupus nephritis and verrucosis of the left ventricle. Besides the findings, the blastogenesis of the patient's lymphocyte was low against stimulation of sac-1 which connects with the Fc portion of lgG, one of the constituent proteins of Staphylococcus. Moreover, anti-phospholipid antibodies turned positive during immunosuppressive therapy and subcutaneous abscess due to Pseudomonas aeruginosae developed concurrently at about the same time, which posed difficulties in the treatment. The affected child had had Staphylococcus aureus infections over a long period of time before diagnosis of SLE and was susceptible to bacterial infections due to Pseudomonas aeruginosae during the treatment. The clinical course of this case was considered important in presuming the complex immunologically abnormal condition of SLE in childhood.
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PMID:[A boy diagnosed SLE after Staphylococcus aureus infection over a long period]. 1128 Sep 1

Forty isolates of rapidly growing Mycobacteria, Mycobacterium fortuitum group including M. fortuitum and M. peregrinum and M. chelonae group including M. chelonae subsp. chelonae and M. chelonae subsp. abscessus at Showa University Fujigaoka Hospital collected between February 1981 and December 1997 were investigated in this study. These isolates were from the patients who were not infected with HIV. The average age of fourteen patients, from whom M. fortuitum group was isolated, was 58 years, ranging from 17 to 80 years old. One patient (71-year-old) with chronic myelogenous leukemia and another (64-year-old) with chronic diabetes mellitus were diagnosed with skin abscesses of M. fortuitum group, which were located on the right site of the neck and in the scar after injecting insulin (injection abscess), respectively. The average age of twenty-six patients, from whom M. chelonae group was isolated, was 57 years, ranging from 32 to 84 years old. One patient (75-year-old) with articular rheumatism was diagnosed with a lung infection of mixed M. chelonae group and Pseudomonas aeruginosa, and another (74-year-old) with diabetes mellitus and kidney failure was strongly suspected of a lung infection. The isolates of the two mycobacteria from the remaining patients were due to colonization, while these patients had the following underlying diseases contributing to infections: pulmonary emphysema; diabetes mellitus; leukemia; collagen diseases; lung cancer; chronic kidney diseases; systemic lupus erythematosus; carcinomatous pleurisy; bronchiectasis; post-tuberculosis. Most isolates of the two mycobacteria were separated from the specimens of patients' respiratory tracts, but since M. chelonae group was a contaminant in the tap-water for diluting concentrated chlorhexidine, the organism happened to be isolated with the mucous membranes of the 6 patients' colons that were picked up while using the washed fiber-scope. These findings suggest that M. fortuitum and M. chelonae groups, in spite of the fact that they rarely cause infection, have a significant risk of infecting aged patients in general hospitals with various underlying diseases attributable to infections. As only a few colonies were isolated from patients' specimens in the majority of cases, it took time to carry out these clinical examinations, and to improve this "laboratory's delay", it is needed to make faster report to clinicians.
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PMID:[Evaluation of rapidly growing Mycobacteria isolates in a general hospital: reports from the hospital microbiology laboratory]. 1144 97

Patients with systemic lupus erythematosus (SLE) have increased susceptibility to infection by Pneumocystis carinii, but this condition has rarely been reported in Taiwan. Here, we describe two cases of patients with SLE who developed Pneumocystis carinii pneumonia (PCP). The first patient was a 39-year-old woman presenting with fever and dyspnea that had lasted 2 weeks. Chest roentgenography disclosed bilateral interstitial and alveolar infiltrates. The second patient was a 22-year-old woman presenting with a 4-day history of malaise, cough, dyspnea, and fever. She had concomitant Mycobacterium tuberculosis infection. Both patients had been treated with varying doses of corticosteroids and/or cytotoxic drugs within 4 months before presentation. Diagnosis was established based on the findings of bronchoalveolar lavage (BAL) and transbronchial lung biopsy (TBLB). Both patients received trimethoprim-sulfamethoxazole (20 mg.kg-1.d-1 trimethoprim), but finally died of nosocomial septicemia (Acinetobacter baumanni and Pseudomonas aeruginosa bacteremia in one, P. aeruginosa bacteremia in the other). These two cases demonstrate that PCP should be included in the differential diagnosis of patients with SLE presenting with pneumonic processes. In addition, a second opportunistic pathogen should be suspected. Bronchoscopic examination should be performed if the diagnosis is not clear and should include TBLB and BAL.
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PMID:Pneumocystis carinii pneumonia in systemic lupus erythematosus: a report of two cases. 1176 Mar 77

We report a patient who developed SLE during the course of diffuse panbronchiolitis (DPB) and had candidiasis later. The patient fulfilled the criteria for diagnosis of SLE after appearance of fever and general peripheral arthritis. Regarding serum virus antibody values at the time of SLE diagnosis, IgG and IgM of human Parvovirus B19 (B19) were positive by the EIA test and also by the serum PCR test. For continuously Pseudomonas aeruginozae in sputum cultures because of existing DPB, immunosuppressasnt therapy with prednisolone and mizoribine was given while suppressing proliferation of bacterial infections with antibiotics. As a result, the intensity of SLE decreased smoothly. About 1 month after beginning of the treatment, the chest X-ray revealed infiltrative densities in the lingual area of the left lobule and in S3 of the right lobule. Judging from the clinical course and various examination findings, concurrence of candidiasis was suspected. Fungal infection in this patient was progressive, so various antifungal agents were used concurrently. Furthermore, immunoglobulin therapy was supplemented while determining serum immunoglobulin levels, and doses of prednisolone and mizoribine were reduced rapidly. Afterward the patient followed a satisfactory clinical course. About 2 years later SLE recurred, aspergillosis developed concurrently and the disease progressed rapidly to its termination. DPB itself is difficult to control and often complicated with various diseases. Therefore, immunosuppresant therapy for complications is sometimes used in addition to the treatment of DPB. More careful observations on the clinical course are necessary in dealing with this disease.
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PMID:[A case of diffuse panbronchiolitis with SLE complicated by fungal infection]. 1176 80

Autoantibodies to the ribosomal phospho (-P) proteins P0, P1, and P2, collectively referred to as Rib-P, are specifically found in 10-40% of patients with systemic lupus erythematosus (SLE). These antibodies are believed to be correlated with lupus nephritis, hepatitis, and central nervous system involvement. The major immunoreactive epitope of these ribosomal antigens has been localized to the carboxy terminus, which is a highly conserved domain of all three proteins and contains two phosphorylated serine residues. The phosphorylated amino acids of the P proteins are known not to be critical epitope determinants. Furthermore, epitope-mapping studies have shown that the major epitope is located within the last 11 C-terminal amino acids. Using peptide arrays we identified more precisely this shared epitope as the six C-terminal amino acids GFGLFD and elucidated the molecular recognition events of anti-Rib-P antibodies at the amino acid level. We identified Phe(111) and Phe(114) of Rib-P2 as the key residues for the interaction, with further contributions of Gly-112 and Asp-115. This amino acid stretch is also present in proteins of several pathogenic micro-organisms such as Trypanosoma cruzi, Brugia malayi, Pseudomonas aeruginosa, Candida albicans, several Leishmania species, and Bartonella henselae. Using newly developed ELISA systems with a C-terminal peptide (C22) and the recombinant proteins (P0, P1, and P2) as antigens we found a high specificity of anti-Rib-P antibodies for SLE and demonstrated positive correlations with anti-U1-C, anti-Sm-B/B' and anti-D and anti-dsDNA antibodies. The sensitivity and specificity in the peptide (C22) based assay varied between 12.8%/100% and 23.4%/96.7% for SLE, depending on the assigned cutoff. In contrast to other studies, we found no significant correlation of anti-Rib-P reactivity with central nervous system manifestations or renal involvement in SLE patients. We conclude that the epitope motif GFGLFD in the C-termini of the ribosomal P proteins is the key determinant of anti-Rib-P antibodies, and that the C22 peptide and the recombinant proteins can be used equally well for the detection of anti-Rib-P antibodies. The role of the major Rib-P epitope in the development of anti-ribosomal P antibodies and in the pathogenesis of SLE remains a subject of further investigation.
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PMID:Characterization of the human autoimmune response to the major C-terminal epitope of the ribosomal P proteins. 1268 28

An 11-year-old boy with consecutive development of systemic lupus erythematosus (SLE) and Wegener granulomatosis (WG) is presented. He was first admitted to the hospital with the findings of SLE, including crescentic glomerulonephritis, Coombs' test-positive hemolytic anemia, hypocomplementemia, antinuclear antibody (ANA) positivity, and elevated levels of anti-double-stranded (ds) DNA antibodies. He was treated successfully with steroids, cyclophosphamide, and peritoneal dialysis. One month after his discharge he developed an apparent viral infection. Three weeks afterwards he was readmitted with the findings of lower respiratory tract involvement, maxillary sinusitis, nasal septum perforation, p- and c-antineutrophil cytoplasmic antibody (ANCA) positivity, but normal complement, ANA, and anti-ds DNA levels, suggesting the diagnosis of WG. He did not respond to anti-infectious and immunosuppressive treatment, and he died of Pseudomonas sepsis.
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PMID:A boy with consecutive development of SLE and Wegener granulomatosis. 1474 Feb 84

In some children with cystic fibrosis (CF), percutaneous long lines occlude sooner than expected (due to thrombophlebitis or thrombosis), and many have a totally implantable venous access device (TIVAD), a recognized complication of which is thrombosis. This complication is more likely if the child has an underlying thrombotic tendency, which may be enhanced in the presence of inflammatory lung disease. There are no reports of an identified association of heritable thrombophilia with CF, although individual cases have been recognized. Our aim was to determine the incidence of thrombophilia in children with CF. In a tertiary pediatric CF center, blood was screened for thrombophilia at annual review, and retested if abnormal. A thrombotic abnormality was found in 41/204 (20%) patients. These included activated protein C resistance (10/204, 5%) with a prevalence similar to that expected, but the following abnormalities had an increased prevalence: antithrombin deficiency (2/204, 1%), protein S deficiency (11/204, 5%), protein C deficiency (8/204, 4%), and lupus anticoagulant (18/204, 9%). There were no differences found in those with thrombophilia for the following parameters: age, gender, genotype, lung function, presence of Pseudomonas aeruginosa, prothrombin time, serum IgE, aspergillus-specific IgE, liver function, and blood inflammatory markers. Fifteen children had TIVADs, 4 of whom had evidence of thrombophilia. In conclusion, a significant proportion of patients had a thrombophilic abnormality. We recommend that thrombophilia screening be performed prior to insertion of a TIVAD, and also in those with a history of venous thrombosis, blocked TIVADs, or recurring problems with long lines.
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PMID:Thrombophilia in children with cystic fibrosis. 1567 7

We report a 37-year-old African-American man with systemic lupus erythematosus (SLE) diagnosed in May 2001 when he presented with biopsy-proven nephritis. He had been treated intermittently from May 2001 to November 2004 with intravenously (i.v.) administered cyclophosphamide and high doses of prednisone due to unrelenting proteinuria. In November 2004, he was admitted to the hospital because of deterioration of renal function and massive proteinuria (21 g dl(-1) 24 h(-1)) and treated with pulses of methylprednisolone and two courses of i.v. administered cyclophosphamide. His hospital course was complicated by cellulitis and bacteremia with Pseudomonas spp. and Streptococcus bovis. He was discharged on prednisone 60 mg daily, ciprofloxacin, augmentin, and hemodialysis. He was readmitted a week later with new onset of seizure activity, slurred speech, and left-sided hemiparesis. Magnetic resonance imaging of the brain revealed multiple ringlike enhancing foci in the frontal and occipital lobes. Brain biopsy was performed, and Gram stain and initial cultures were negative. Empiric tobramycin, cefepime, and metronidazole were administered. Diagnosis was delayed for several months, but culture eventually grew Nocardia asteroides. Trimethoprim-sulfomethoxazole and linezolid therapy was begun. This was followed by slow, but steady, clinical improvement. Risk factors, diagnostic clues, and treatment are reviewed.
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PMID:Nocardia brain abscesses in a male patient with SLE: successful outcome despite delay in diagnosis. 1668 77

Infection, particularly pneumonia, is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). This study was performed to assess the prevalence, causative organisms, and outcomes of community-acquired pneumonia (CAP) in Thai SLE patients, and determine the predicting factors for death. A retrospective chart review of adult SLE patients, age >16 years, seen at the Division of Rheumatology, Chiang Mai University over an 18 year period was carried out. Cases diagnosed with CAP were selected for this study. Of 542 SLE patients, a total of 56 episodes of CAP occurred in 52 patients. Their mean age +/- SD and duration of SLE were 37.98 +/- 11.48 years and 34.99 +/- 54.53 months, respectively. Thirty-three CAP cases (58.9%) occurred within the first year of diagnosis with SLE. The causative organisms identifiable in 40 patients (71.5%) were Mycobacterium tuberculosis in 12, Nocardia spp in 6, Aspergillus spp in 5, Staphylococcus aureus in 3, Pneumocystis carinii, Haemophilus influenzae, Escherichia coli, and Pseudomonas aeruginosa in 2 each, and Acinetobactor baumanii, Burkholderia pseudomallei, and Strongyloides stercoralis in 1 each. The remaining 3 patients had mixed bacterial infection. The overall mortality rate was 26.8%. Use of high dose prednisolone (> or =15 mg/day), and ventilator support were significantly associated with death.
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PMID:Community-acquired pneumonia in Thai patients with systemic lupus erythematosus. 1787 30

The main objective of this study is to describe the presence of infections in patients with pulmonary haemorrhage and systemic lupus erythematosus. Patients with systemic lupus erythematosus and pulmonary haemorrhage were thoroughly evaluated in the first 48 hours with imaging plus bronchoscopy and bronchoalveolar fluid analysis. If needed, videoassisted thoracoscopy and lung biopsy were performed too. In all, search for bacterial, mycobacterial and fungal infections proceeded. Appropriate blood, bronchoalveolar fluid and tissue cultures were taken. Patients were treated with antibiotics and corticosteroids in case of infection. Otherwise, they received initial intravenous methylprednsiolone pulses for 3 days as standard therapy for pulmonary haemorrhage in systemic lupus erythematosus. Additional treatment with immunosuppressives was further decided by the treating physicians. Fourteen events in 13 patients were evaluated. In eight events (57%), an infection was demonstrated. Aetiological agents included Pseudomonas sp. and Aspergillus fumigatus. Four patients died, three of them because of the pulmonary infection and one because of cerebral haemorrhage secondary to severe systemic hypertension, 48 hours after methylprednisolone treatment. Patients with systemic lupus erythematosus and pulmonary haemorrhage have a high prevalence of infections. The influence of pulmonary haemorrhage in the setting of systemic lupus erythematosus needs further study to establish adequate treatment and to reduce the high mortality of this complication.
Lupus 2008 Apr
PMID:High prevalence of infections in patients with systemic lupus erythematosus and pulmonary haemorrhage. 1841 10


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