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)

Human plasma prekallikrein (Fletcher factor) clotting activity and antigen levels have been examined in various clinical conditions. Prekallikrein antigen was measured by a newly developed, specific, and sensitive radioimmunoassay. The assay had no demonstrable cross-reactivity with human urinary kallikrein nor, in the species tested, animal plasma prekallikrein. This assay was able to measure plasma kallikrein after its biological functions had been inactivated by plasma inhibitors. Normal human pooled plasma contained approximately 50 microgram/ml prekallikrein. Quantitative measurement of plasma prekallikrein was possible for concentrations as low as 0.3% of that of normal pooled plasma. A good correlation (correlation coefficient = 0.71) existed between titers of plasma prekallikrein measured by Fletcher factor clotting assays and radioimmunoassays among 40 normal subjects. Both prekallikrein clotting activity and antigen were significantly reduced in plasmas of patients with advanced hepatic cirrhosis or DIC. Prekallikrein activity and antigen were mildly decreased in plasmas or serums of patients with chronic renal failure and nephrotic syndrome but were normal in those of patients under treatment with warfarin or suffering from SLE, rheumatoid arthritis, sarcoidosis, or HANE. Human cord serum contained a lower titer of prekallikrein antigen than adult serum. Strenuous physical exercise did not significantly change plasma prekallikrein levels.
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PMID:Human plasma prekallikrein (Fletcher factor) clotting activity and antigen in health and disease. 65 66

A radioimmunoassay for fibrinopeptide A (FPA) has been developed. This assay uses rabbit antibodies induced by injection of native FPA-human serum albumin conjugates and 125I introduced into tyrosine-FPA synthesized in out laboratory. Plasma FPA is separated from fibrinogen by TCA extraction. The assay is capable of detecting as little as 50 pg/ml of FPA. In 20 normal donors this assay revealed a mean concentration of 0.9 ng/ml (0.3 SD). In five patients with disseminated intravascular coagulation, FPA concentrations ranged from 13.0 to 346 ng/ml. Two groups of patients with systemic lupus erythematosus (SLE) whose disease had achieved complete remission were studied; one consisted of four patients with no history of lupus nephritis and another with a history of nephritis. Mean FPA concentrations of 1.5 ng/ml (range, 0.7-1.8 ng/ml) and 2.7 ng/ml (range, 1.1-5.6 ng/ml) were found in these two groups, respectively. Another group of nine patients with active SLE, but without evidence of lupus nephritis, had a mean FPA concentration of 4.5 ng/ml (range, 2.4-7.8 ng/ml). Finally, a group of seven patients with active SLE, including active nephritis, had a mean FPA concentration of 10.2 ng/ml (range, 5.3-17.0 ng/ml). A positive correlation was found between the concentration of plasma FPA and serum DNA-binding activity and an inverse correlation was found between plasma FPA and the concentration of serum C3. No correlation existed between plasma FPA and concentration of serum creatinine. Several possibilities for the origin of plasma FPA in patients with SLE were considered; at present it seems most likely that FPA arises through the action of thrombin on fibrinogen.
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PMID:Fibrinopeptide A in plasma of normal subjects and patients with disseminated intravascular coagulation and systemic lupus erythematosus. 93 2

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.
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PMID:Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. 100 85

A case of disseminated intravascular coagulation (DIC) in a patient with systemic lupus erythematosus (SLE) with acute liver dysfunction is described. A 37-year-old man with SLE developed acute DIC and marked liver damage after fracture of the right clavicle and pharyngitis. Treatment with high-dose steroids, heparin, antithrombin III, gabexate mesilate, and antibiotics resulted in prompt improvement. The recovery of an SLE patient after acute DIC and marked liver damage is considered very rare. We report here such a case and discuss the previous reports.
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PMID:Disseminated intravascular coagulation in lupus erythematosus with acute liver damage. 130 Jan 75

Multiorgan thrombotic disorders have been described in a variety of conditions including systemic lupus erythematosus. Among these are the 'catastrophic' antiphospholipid syndrome, disseminated intravascular coagulation and the thrombotic thrombocytopenic purpura-haemolytic uraemic syndrome. In this review we briefly analyse some specific clinical and haematological characteristics of these conditions and attempt to uncover common links between them.
Lupus 1992 Aug
PMID:Multiorgan thrombotic disorders in systemic lupus erythematosus: a common link? 130 83

Pancreatitis in SLE remains an enigma and probably results from multiple pathogenetic mechanisms. However, cases of pancreatic thrombus formation remain few and far between, suggesting that APS is not the major cause of pancreatitis. Whether aPL contribute to pancreatic thrombus formation in rare patients needs to be demonstrated by antemortum arteriographic studies showing thrombus or vasculopathy. The postmortem pancreatic examination of patients who have died of the disseminated vasculopathy-coagulopathy syndrome remains problematic, because if thrombi are found, they may simply represent the endstage of multiple mechanisms, including hypotension, hypoxia, DIC, or TTP, rather than an aPL specific mechanism.
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PMID:Pancreatitis in systemic lupus erythematosus: still in search of a mechanism. 151 54

A 44-year-old woman with a history of systemic lupus erythematosus on no steroid or immunosuppressive medication presented in septic shock complicated by renal failure and disseminated intravascular coagulation. The patient was treated with antibiotics. Liver-spleen scintigraphy with Tc-99m albumin colloid initially failed to reveal tracer accumulation in the spleen. Follow-up study after one year revealed normal tracer uptake in the spleen. The transient blockade of reticuloendothelial system by immune complexes is the most likely mechanism. Other possible mechanisms include disturbed vascular supply due to thrombosis secondary to the disseminated intravascular coagulation or vasculitis.
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PMID:Reversible functional asplenia in systemic lupus erythematosus. 174 31

In order to clarify the abnormalities of blood coagulation and fibrinolysis in patients with various renal diseases, some molecular markers for hemostasis and thrombosis were examined in comparison with those of the patients with disseminated intravascular coagulation. The results were as follows: 1) PIC was significantly higher in the patients with CGN, NS, SLE, HD and DIC than normal subjects. 2) TAT was significantly higher in the patients with CGN, NS, HD and DIC. 3) SFMC was significantly higher only in the patients of DIC. 4) FDP and FDP-E were significantly higher in the patients with HD and DIC. 5) D-dimer was significantly higher in the patients with CGN, CRF, HD and DIC. These results suggested that the abnormalities of blood coagulation and fibrinolysis in patients with various renal diseases are relatively mild, and situated between the normal subjects and patients with DIC.
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PMID:[Studies on molecular markers for hemostasis and thrombosis in various renal diseases]. 183 16

Thrombomodulin (TM) is a constituent glycoprotein of endothelial cell membrane, and soluble TM is present also in plasma and urine. It was revealed by experiments using cultured HUVEC in vitro that TM is released from endothelial cell membrane not with monensin, thrombin, fibroblast growth factor, interleukin-1 or endotoxin, but with H2O2 or endotoxin-treated granulocytes. And the release was suppressed by the coexistence of gabexate mesilate or superoxide dismutase. It was suggested that soluble TM was released from endothelial cell membrane by its injury and digested to multiple molecular forms by endogenous and granulocytic protease(s). TM level in circulation is increased in cases of SLE, MCLS, diabetic angiopathy. It was increased in cases of overt DIC and decreased to the normal level when the patient was recovered from DIC. TM level in circulation was also increased in cases of decompensated liver cirrhosis and markedly in cases of renal insufficiency. It was concluded that plasma TM is a parameter reflecting endothelial injury due to inflammation or metabolic disorders of vascular system. But the interpretation of increased plasma TM was difficult when renal insufficiency was complicated.
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PMID:[Soluble thrombomodulin: a specific parameter of endothelial injury]. 185 Dec 35

A 28-year-old female patient with SLE was found to have complications from intrauterine fetal death, eclampsia, and brainstem vascular damage during pregnancy. These symptoms were associated with lupus anticoagulant (LAC). An LAC positive SLE case with accompanying cerebrovascular disease and fetal loss at the same time has rarely been reported. The first brain CT scan revealed the presence of multiple middle pons infarction. Ten days after onset, a brain MRI showed the change into hemorrhagic infarction in the same region, suggesting disseminated intravascular coagulation (DIC) caused by severe obstetric complications. Although the severity of the brain damage implied poor prognosis, her symptoms were alleviated by intensive care with a large amount of steroid therapy and active rehabilitation. LAC-positive SLE patients are apt to encounter obstetric complications in pregnancy. Therefore they must be treated by medical specialists in cooperation with gynecologists. When they also have accompanying with cerebrovascular diseases, active therapy for SLE is necessary for a good prognosis.
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PMID:[A case of pregnant woman with lupus anticoagulant positive systemic lupus erythematosus complicated with intrauterine fetal death, eclampsia, and brainstem vascular damage]. 192 97


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