<\/p>\n
<\/p>\n
<\/p>\n
ana, c3, c4, hepatitis panel, UA, CRP, ESR<\/p>\n
Joint pain, fever, and rash<\/p>\n
Proteinuria, pericardititis, pleural effusions, GI, excess clotting due to lupus anticoag<\/p>\n
Need 4 of 11 criteria:<\/p>\n
Pleuritis–convincing history of pleuritic pain or rub heard by a physician or evidence of pleural effusion<\/p>\n
Pericarditis–documented by electrocardiogram or rub or by evidence of pericardial effusion<\/li>\n
Persistent proteinuria >0.5 g\/day or >3+ if quantitation not performed<\/p>\n
Cellular casts–may be red cell, hemoglobin, granular, tubular, or mixed<\/li>\n
Seizures–in the absence of offending drugs or known metabolic derangements, e.g., uremia, ketoacidosis, or electrolyte imbalance<\/p>\n
Psychosis in the absence of offending drugs or known metabolic derangements, e.g., uremia, ketoacidosis, or electrolyte imbalance<\/li>\n
Hemolytic anemia with reticulocytosis<\/p>\n
Leukopenia <4000\/mm3 total on two or more occasions<\/p>\n
Lymphopenia <1500\/mm3 on two or more occasions<\/p>\n
Thrombocytopenia <100,000\/mm3 in the absence of offending drugs<\/li>\n
Anti-DNA: antibody to native DNA in abnormal titer<\/p>\n
Anti-Sm: presence of antibody to Sm nuclear antigen<\/p>\n
False-positive serologic test for syphilis known to be positive for at least 6 mo and confirmed by Treponema pallidum<\/em> immobilization or fluorescent treponemal antibody absorption test<\/p>\n Antinuclear antibody<\/li>\n<\/ol>\n Pt with SLE, fever and urinary retention = Myelitis, treat with high dose steroids<\/p>\n necrotizing granulomatous disease effecting lungs and kidney.\u00a0 C-Anca<\/p>\n <\/p>\n DISCUSSION<\/strong> Wegener\u0092s granulomatosis (described by the German pathologist Friedrich Wegener in 1939)1<\/a> is a multisystem granulomatous conditionof unknown aetiology. It is defined by the American Collegeof Rheumatology as the presence of two of four clinopathologicalcriteria2<\/a>(box).<\/p>\n ENT problems are found in 80% of patients and give the mainclue to the diagnosis.3<\/a> Those that may present in the emergencydepartment include stridor from subglottic stenosis, oral ulceration,sinusitis, otitis media and sudden conductive or sensorineuraldeafness.4<\/a> Necrosis of vessels in the cartilaginous septum leadsto epistaxis, septal perforation and eventually a saddle-nosedeformity.<\/p>\n Depending on the history, an ENT examination and chest radiograph or urine analysis should be performed. If characteristic abnormalitiesare found, the next step is either nasal or renal biopsy (the gold standard) or PR3 ANCA testing. In Wegener\u0092s granulomatosis, autoantibodies are directed at proteinase 3, a proteinase foundin the granules of neutrophils. Meta-analysis has showen thesensitivity of PR3 ANCA for active Wegener\u0092s is 91% andspecificity 99%.5<\/a> However, a small number of patients with vasculitidessuch as microscopic polyangiitis and Churg\u0096Strauss syndromemay test positive for PR3 ANCA.6<\/a> In addition, a positive PR3ANCA may only be expressed late on in the disease. Hence, we suggest that in patients with active, severe disease who presentto an emergency department, autoantibody testing should be usedearly, as it is more likely to show an abnormality. Biopsy canbe performed once the patient is stable.<\/p>\n Fulminant disease may require dialysis, plasma exchange and, unlike other vasculitides, cyclophosphamide, making an accurate diagnosis important. Before its introduction, the median timefrom presentation to death was 5 months, typically from necrotising glomerulonephritis.7<\/a> This highlights the need to perform urineanalysis in patients with unusual ENT symptoms.<\/p>\n <\/p>\n Classification criteria for Wegener\u0092s granulomatosis (sensitivity88%, specificity 92%)<\/strong><\/p>\n <\/p>\n<\/span>Wegener’s:<\/span><\/h2>\n