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)

Severe infections are a common cause of death in patients suffering from systemic lupus erythematosus (SLE). We here report on a fatal multidrug-resistant Acinetobacter baumannii sepsis in a patient with newly diagnosed SLE, who had to be treated with immunosuppressants due to lupus nephritis. Detailed analysis of the patient's history revealed that colonisation probably had occurred during a recent hospitalisation of the patient in the Mediterranean region. E-test analysis indicated that resistance to carbapenems was mediated by a plasmid-encoded metallo-beta-lactamase. We conclude that travel history including previously visited health care facilities always should be carefully considered for decisions on anti-infective therapy, as travel activities increasingly facilitate spread of antimicrobial resistances.
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PMID:Fatal multidrug-resistant Acinetobacter baumannii sepsis in a patient with travel history and recent onset of systemic lupus erythematosus: a case report. 1681 54

The G protein-coupled receptor (GPCR) G2A (for G2 accumulation) was identified as a stress-inducible antiproliferative cell cycle regulator. Targeted G2A gene deletion in mice resulted in systemic lupus erythematosus-like and atherosclerotic lesion phenotypes. These findings suggested that G2A may be a therapeutic target for cancers and autoimmune and cardiovascular diseases. The G2A receptor is cytotoxic upon ectopic expression, and its cognate ligand has not been identified, making it difficult to generate a cell line for screening using a conventional approach. The function of human G2A remains obscure. Here we show that by using an inducible T-REx (Invitrogen, Carlsbad, CA) expression system an inducible G2A functional cell-based beta-lactamase reporter assay could be developed using the constitutive activity of the receptor. Furthermore, G2A expression levels can be controlled under this inducible system to avoid the expression artifacts of conventional approaches using constitutive expression vectors. This stable cell line expressing the human G2A receptor was screened against a chemical library containing 740,000 compounds, and small molecules showing selective agonistic activity on G2A were identified. We believe the strategy employed here for G2A should be applicable to other "intractable" GPCRs where target gene expression results in cytotoxic and/or high constitutive activities.
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PMID:Agonists of the orphan human G2A receptor identified from inducible G2A expression and beta-lactamase reporter screen. 1950 30

Most common bacterial species causing peritonitis in the course of peritoneal dialysis (PDP) are coagulase-negative staphylococci, Staphylococcus aureus and streptococci. Haemophilus influenzae is rarely associated with PDP. Hereby we present the first known case of APD-associated peritonitis caused by non-type able H. influenzae (NTHi) presenting the beta-lactamase negative, ampicillin-resistant (BLNAR) phenotype. An 18 year old boy who had been treated with the APD for 12 months due to SLE was admitted in good general condition with diagnosis of PDP. Standard diagnostic and therapeutical procedures were initiated. Dialysis fluid was turbid with cytosis of 435 WBC/ml. From dialysis fluid pure culture of Gram-negative coccobacillus was isolated. The isolate was identified as a BLNAR phenotype. The same bacterium was isolated from nasal swab. Blood cultures were negative. After evaluation of antimicrobial susceptibility the treatment was changed for the oral ciprofloxacin. The treatment was successful. Control tests 2 days later revealed cytosis of 15 WBC/mm3 and control cultures of peritoneal fluid were negative. After two weeks of treatment the patient was discharged in a good condition. Haemophilus influenzae is a bacterium frequently colonizing the nasopharyngeal cavity. A PCR-based method allowed to classify isolates as NTHi. Infection was probably of the respiratory origin as the isolates (from peritoneal fluid and nasal swab) were undistinguishable. There are only few reports describing this species as an ethiologic agent of peritonitis. This case prove that Haemophilus species should be taken into account as a possible aethiologic agent of PDP, especially in patients on immunosupression with carrier state of H. influenzae in the upper respiratory tract. This kind of microorganism requires specific conditions during its growing in vitro. Identification of its sensitivity to antibiotics is essential in order to detect strains of BLNAR phenotype, as it is a crucial part of an effective antibiotic therapy.
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PMID:[Peritonitis in the course of peritoneal dialisis caused by Haemophilus influenzae with BLNAR phenotype]. 1958 Feb

Infections in lower extremities are sometimes concerned with systemic immunological disorders such as idiopathic thrombocytopenic purpura and systemic lupus erythematosus, which are treated with systemic steroids. Steroid therapy impairs the epithelial wound healing and with systemic condition, especially with systemic lupus erythematosus, the wound is susceptible for infection. Even a pyoderma gangrenosum sometimes occurs in a patient with idiopathic thrombocytopenic purpura with an incisional wound of hernia. The severe signs and symptoms are the deep skin and soft tissue infections, mainly caused by group A streptococcus, composed of necrotizing fasciitis and muscle necrosis. Medically suspected necrotizing fasciitis patients should be empirically and immediately administered with broad-spectrum antibiotics, which may cover the common suspected pathogens. In type I (polymicrobial) infection, the selection of antimicrobial should be based on medical history and Gram staining and culture. The coverage against anaerobes is important in type I infection. Metronidazole, clindamycin, or beta-lactams with beta-lactamase inhibitor or carbapenems are the treatment of choice against anaerobes, while early surgical debridement-wide enough and deep enough-is the core treatment of necrotizing fasciitis and results in significantly better mortality compared with those who underwent surgery after a few hours of delay. When necrotizing fasciitis is considered and the patient is brought to the operation room, aggressive and extensive surgical debridement is explored. Tissue involved should be completely removed until no further evidence of infection is seen. When further debridement is required, the patient must return to the operating room immediately. In this context, the temporal coverage using the artificial dermis after debridement is useful because there is no loss of the patient's own tissue and yet it is easier for "second-look" surgery or secondary reconstruction, and extensive enough debridement is always the mainstay of the therapy.
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PMID:Lower Extremity Wounds in Patients With Idiopathic Thrombocytopenic Purpura and Systemic Lupus Erythematosus. 2635 24