Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum FDPs were investigated in 30 healthy and 95 patients with pulmonary thrombembolia, not-stabilized angina pectoris, myocardial infarction, rheumatism, rheumatoid arthritis, lupus erythematodes and dermatomyositis. FDPs are determined by hemagglutination inhibition according to Merskey. They are found in the sera of the healthy in average values of 3.73 mkgr/ml. The highest average values in the first 24 h were found in case of pulmonary thrombembolia up to 106.64 mkgr/ml, followed by rheumatoid arthritis 26.3 mkgr/ml, myocardial infarction with complication 22.4 mkgr/ml, rheumatism +5.58 mkgr/ml, not-stabilized angina pectoris 5.5 mkgr/ml; and noncomplicated myocardial infarction 4.3 mkgr/ml. By the third day of the disease FDP in pulmonary thrombembolia decreased, whereas a negligible elevation was observed in case of non-complicated myocardial infarction. The results were interpreted as well as the cause for the presence of the mentioned products in those groups of diseases. FDP determination is recommended as a routine method in case of: diagnosis of pulmonary thrombembolia, differentiation of myocardial infarction with or without complications, differentiation of pulmonary thrombembolia from myocardial infarction in emergency states, progressing with chest pain, collapse phenomena, dyspnea and establishment of the activity of the process of rheumatoid arthritis. FDP determination in stenocardia and rheumatism is not expedient.
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PMID:[Level of fibrinogen/fibrin degradation products (F/FDP) in certain internal diseases]. 49 29

Ninety-five patients with steroid-induced avascular necrosis of bone have been personally treated by the author. Of these, eighteen had a lesion of the head of the humerus, on one or both sides. The conditions for which the steroids were given included post-transplantation, lupus erythematosus, glomerulonephritis and asthma. The characteristic lesion began as a subchondral osteolytic area which frequently progressed to collapse. The articular cartilage divided from the subchondral bone, either becoming detached as a free cap or at a later stage reattaching. In some cases the lesion was minimal and the symptoms were slight. Conservative treatment has consisted of pendulum exercises and avoidance of abduction, particularly against resistance. In fourteen patients this led to satisfactory function with only intermittent symptoms. Four patients required replacement of five humeral heads with Neer's prostheses. After one to seven years the results of all five were classified as excellent in terms of absence of symptoms and a free range of movement.
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PMID:Steroid-induced avascular necrosis of the head of the humerus. Natural history and management. 95 47

Recent reports of avascular necrosis (AN) in systemic lupus erythematosus (SLE) have suggested that its occurrence may be most frequent in young patients. In our population of 99 patients with SLE, 7 young patients have developed AN. Patterns of prednisone therapy had no apparent relationship to the development of AN. AN may become apparent in patients who have relatively inactive lupus, when increased physical activity precipitates articular collapse. A diagnosis of AN should be considered in young patients with localized joint pain.
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PMID:Avascular necrosis in SLE. An apparent predilection for young patients. 98 3

Should rheumatologists provide an acute referral service for general practitioners (GPs) and other clinical units? Is it cost effective? We prospectively studied acute referrals to one unit over 10 months, recording their source, diagnosis, management and outcome. Current rheumatology patients and cases only needing telephone advice were excluded. There were 253 referrals: 82 from GPs, nine from Accident and Emergency, and 162 from other hospital units. Their diagnoses comprised connective tissue diseases (22), back pain (46), inflammatory arthritis (59), osteoarthritis (22), paediatric cases (11), soft tissue problems (41) and 52 other disorders. Thirty-two needed active treatment within 24 h (classified as emergencies); examples included cerebral lupus, vasculitic pulmonary haemorrhage, retroperitoneal lymphoma with sacral plexus compression, temporal arteritis with reduced visual acuity and acute monoarthritis. All needed immediate therapy; only one died. Most (176 cases) were less urgent and needed advice in 48 h. Examples included osteoporotic vertebral collapse and acute rheumatoid disease. Forty-five could have been seen routinely; examples included lateral epicondylitis and adhesive capsulitis. The service required 1 day per week of medical staff time at an average cost of 45 pounds per case. We concluded that an acute rheumatology service is needed; it can be provided within the working day and is cost effective.
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PMID:The clinical need for an acute rheumatology referral service. 862 47

We describe a case of active systemic lupus erythematosus (SLE) complicated with a large amount of pericardial effusion with diastolic collapse of right ventricle suggestive of tamponade. Isolates from surgical drainage of pericardial fluid showed Acinetobacter baumannii exhibiting multiple antibiotics resistance. Despite the high frequency of both pericardial involvement and of infection complications in SLE, septic pericarditis and tamponade is considered rare. Most of the reported cases of septic pericarditis in SLE were due to Staphylococcal aureus, and Acinetobacter baumannii has never been reported before.
Lupus 1997
PMID:Acinetobacter pericarditis with tamponade in a patient with systemic lupus erythematosus. 922 70

The case of a patient with systemic lupus erythematosus (SLE) is reported which was accompanied by renal dysfunction and massive vascular immune deposits in the kidney without active glomerular lesions. The renal biopsy showed arterioles and small arteries with circumferential periodic acid-Schiff (PAS) and Masson trichrome-positive homogenous material in the subendothelial area in the absence of thrombotic, necrotizing or inflammatory lesions. Immunofluorescence and electron microscopy examination demonstrated immune deposits in the vascular walls. Glomeruli showed only minor abnormalities with a trend to collapse. There was no improvement in renal dysfunction over a 4-year period until the patient's death, despite steroid therapy producing a decrease in disease activity. The autopsy showed similar vascular changes to those seen in the biopsy, however; glomeruli were either sclerotic or showed a trend to collapse. Massive uncomplicated vascular immune complex deposition without active glomerular lesions is rare. The present case indicates that this type of lupus vasculopathy may be a prognostic factor for the loss of renal function in SLE mediated by hemodynamic glomerular injury.
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PMID:Massive uncomplicated vascular immune complex deposits in the kidney of a patient with systemic lupus erythematosus. 934 93

The various phospholipid classes that comprise mammalian cell membranes are distributed over both leaflets of the bilayer in a non-random fashion. While a specific and ATP-dependent transporter is responsible for rapid inward movement of aminophospholipids, its inhibition does not lead to spontaneous redistribution of lipids. Conditions of cellular activation which are accompanied with increased levels of intracellular Ca2+ may cause a collapse of lipid asymmetry by switching on an ATP-independently operating scramblase, which accelerates bidirectional movement of all phospholipid classes. The most prominent change in transmembrane lipid distribution is surface exposure of phosphatidylserine (PS), the more so since conditions which activate scramblase in most if not all cases lead to inhibition of aminophospholipid translocase activity, which will prevent PS from being pumped back to the inner leaflet of the membrane. Surface-exposed PS serves at least two important physiological functions: it promotes blood coagulation and offers a recognition signal for clearance by macrophages and other cells of the reticuloendothelial system. As such, PS exposure may form an important early event in the process of apoptosis to ensure rapid removal of these cells in order to avoid release of their inflammatory contents. Defective regulation of transbilayer lipid distribution may result in clinical manifestations such as in the Scott syndrome, a bleeding disorder caused by an impaired scramblase activity. Conversely, excessive PS exposure may lead to thrombosis or may explain formation of so-called antiphospholipid antibodies as occurring in patients with antiphospholipid syndrome.
Lupus 1998
PMID:Regulatory mechanisms of transmembrane phospholipid distributions and pathophysiological implications of transbilayer lipid scrambling. 981 89

A 51-yr-old woman developed pulmonary embolism while undergoing surgery for breast cancer with Auchincloss method. General anesthesia was maintained with propofol and fentanyl. The course of anesthesia and operation were uneventful until the skin was sutured, when unexplained severe circulatory collapse developed. A widely dissociated EtCO2-PaCO2 suggested pulmonary embolism. The pulmonary circulation was restored 10 minutes after the start of heparin therapy, and the intravenous heparin administration was continued. The patient was extubated uneventfully 24 hours postoperatively. Lung perfusion scintigrams showed defect in right lower lungs (S 6, S 9). Venograms of the lower extremity disclosed thrombosis of the right popliteal vein. Furthermore, lupus anticoagulant was noted in the serum. Patients with antiphospholipid syndrome often develop pulmonary complications including pulmonary embolism and pulmonary hypertension. Intra-operative pulmonary embolism associated with lupus anticoagulant is a rare case.
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PMID:[A case of intraoperative pulmonary embolism associated with lupus anticoagulant]. 1107 59

The properties of a proapoptotic 1,4-benzodiazepine, Bz-423, identified through combinatorial chemistry and phenotype screening are described. Bz-423 rapidly generated superoxide (O(2)(-)) in transformed Ramos B cells. This O(2)(-) response originated from mitochondria prior to mitochondrial transmembrane gradient collapse and opening of the permeability transition pore. Bz-423-induced O(2)(-) functioned as an upstream signal that initiated an apoptotic program characterized by cytochrome c release, mitochondrial depolarization, and caspase activation. Pretreatment of cells with agents that either block the formation of Bz-423-induced O(2)(-) or scavenge free radicals attenuated the death cascade, which demonstrated that cell killing by Bz-423 depends on O(2)(-). Parallels between Ramos cells and germinal center B cells prompted experiments to determine whether Bz-423 had therapeutic activity in vivo. This possibility was tested using the (NZB x NZW)F(1) murine model of lupus, in which the pathologically enhanced survival and expansion of germinal center B cells mediate disease. Administration of Bz-423 for 12 weeks specifically controlled germinal center hyperplasia and reduced the histological evidence of glomerulonephritis. Collectively, these studies define a new structure-function relationship for benzodiazepines and point to a new target and mechanism that could be of value for developing improved drugs to manage systemic lupus erythematosus and related disorders.
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PMID:Benzodiazepine-induced superoxide signals B cell apoptosis: mechanistic insight and potential therapeutic utility. 1239 48

Post-infectious glomerulonephrites (GNs) include a wide spectrum of nephropathies, with known etiological agent, bacterial, parasitic, viral. Among GNs secondary to bacterial infections, post-streptococcal GN is the most frequent; nevertheless, its incidence in developed countries has decreased during the last 20 years, while some of the characteristics such as types of infection, exposed subjects, clinical and evolutionary patterns have changed. Prognosis has worsened and is correlated with some clinical and histological parameters. The viral infection-related GNs include those associated with HBV, HCV, HIV plus other rarer forms. Membranous GN (MGN), membranoproliferative GN (MPGN) and IgA nephropathy may occur in the course of HBV infection, while different GNs can be detected in relation to HCV, the most frequent being mixed cryoglobulinemic GN, a MPGN with peculiar morphological features. Multiple glomerular involvements are seen from HIV infection, the more characteristic form being the so-called HIV associated nephropathy (HIVAN), a focal segmental glomerulosclerosis with tuft collapse affecting African subjects, which starts with a nephrotic syndrome and rapidly develops into uraemia. Other GNs derive from HIV-related immunecomplexes, some with diffuse proliferative characteristics, or lupus like, with less severe clinical manifestations compared with HIVAN. Among the rare viral infections, we ultimately, mention the association between Parvovirus B19 and "collapsing" focal segmental glomerulosclerosis.
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PMID:[Post-infectious glomerulonephritis]. 1274 5


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