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)

The role of thrombophilia in the pathogenesis of preeclampsia is controversial. The aim of this case-controlled study was to determine whether thrombophilia increases the risk of preeclampsia or interferes with its clinical course. A total of 808 white patients who developed preeclampsia (cases) and 808 women with previous uneventful pregnancies (controls) matched for age and parity were evaluated for inherited and acquired thrombophilia (factor V Leiden; factor II G20210A; methylenetetrahydrofolate reductase C677T; protein S, protein C, and antithrombin III deficiency; anticardiolipin antibodies; lupus anticoagulant; and hyperhomocysteinemia). Odds ratios (ORs) with 95% confidence intervals (CIs) for risk of being carriers of thrombophilia in cases compared with controls and for risk of maternal life-threatening complications and adverse perinatal outcomes in preeclamptic patients with or without thrombophilia were calculated. Women with severe preeclampsia (406 cases) had a higher risk (OR, 4.9; 95% CI, 3.5 to 6.9) of being carriers of either an inherited or acquired thrombophilic factor, except for protein S, protein C, and antithrombin deficiency. In women with mild preeclampsia (402 cases), only prothrombin and homozygous methylenetetrahydrofolate reductase gene mutations were significantly more prevalent than in the controls. Thrombophilic patients with severe preeclampsia are at increased risk of acute renal failure (OR, 1.8; 95% CI, 1.5 to 2.2), disseminated intravascular coagulation (OR, 2.7; 95% CI, 1.1 to 6.4), abruptio placentae (OR, 2.6; 95% CI, 1.2 to 6.0) and perinatal mortality (OR, 1.7; 95% CI, 1.5 to 2.2) compared with nonthrombophilic preeclamptic patients. Our study demonstrates a significant association between maternal thrombophilia and severe preeclampsia in white women. Thrombophilia also augments the risk of life-threatening maternal complications and adverse perinatal outcomes in preeclamptic patients.
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PMID:Thrombophilia is significantly associated with severe preeclampsia: results of a large-scale, case-controlled study. 1628 82

There is ample evidence suggesting that hepatitis C virus (HCV)-associated autoimmunity plays a role in a broad spectrum of autoimmune diseases, which are usually overlooked. We report on a case of nephrotic syndrome, palpable purpura, cryoglobulinemia, hypocomplementemia, and acute renal failure complicated by immune complex glomerulonephritis (GN). The patient is a 64-year-old man with HCV infection, who was initially considered to present only an HCV-associated cryoglobulinemic GN. However, renal biopsy revealed a "full house" immune complex crescentic GN, which led to our subsequent investigation. The attending clinicians faced what is a common dilemma, where an HCV-associated autoimmune disease inevitably switches to a lupus-like GN. Hence, we also discuss treatment.
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PMID:HCV infection complicated with nephrotic syndrome, immune complex crescentic glomerulonephritis and acute renal failure: a case report. 1630 51

Lung and kidney function are intimately related in both health and disease. Respiratory changes help to mitigate the systemic effects of renal acid-base disturbances, and the reverse is also true, although renal compensation occurs more slowly than its respiratory counterpart. A large number of diseases affect both the lungs and the kidneys, presenting most often with alveolar hemorrhage and glomerulonephritis. Most of these conditions are uncommon or rare, although three of them--Wegener's granulomatosis, systemic lupus erythematosus, and Goodpasture's syndrome--are not infrequently encountered by respiratory care clinicians. Respiratory complications of chronic renal failure include pulmonary edema, fibrinous pleuritis, pulmonary calcification, and a predisposition to tuberculosis. Urinothorax is a rare entity associated with obstructive uropathy. Sleep disturbances are extremely common in patients with end-stage renal disease, with sleep apnea occurring in 60% or more of such patients. The management of patients with acute renal failure is frequently complicated by pulmonary edema and the effects of both fluid overload and metabolic acidosis. These processes affect the management of mechanical ventilation in such patients and may interfere with weaning. Successful lung-protective ventilation in patients with acute lung injury and renal failure may require modification of hemodialysis in order to combat severe acidemia. Hemodialysis-related hypoxemia, which was once believed to be the result of pulmonary leukostasis and complement activation, is explained by diffusion of CO2 into the dialysate, with concomitant alveolar hypoventilation in the process of maintaining a normal P(aCO2). Like acute lung injury, renal failure is a common complication of critical illness. An increasing body of evidence also supports the notion that the kidneys, like the lungs, are susceptible to injury induced as a result of positive-pressure mechanical ventilation.
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PMID:Respiratory considerations in the patient with renal failure. 1656 95

Haemolytic uraemic syndrome (HUS) is the most common cause of acute renal failure in children. The syndrome is defined by triad of microangiopathic haemolytic anaemia, thrombocytopenia and acute renal failure (ARF). Incomplete HUS is ARF with either haemolytic anaemia or thrombocytopenia. HUS is classified into two subgroups. Typical HUS usually occurs after a prodrome of diarrhoea (D+HUS), and atypical (sporadic) HUS (aHUS), which is not associated with diarrhoea (D-HUS). The majority of D+HUS worldwide is caused by Shiga toxin-producing Esherichia coli (STEC), type O157:H7, transmitted to humans via different vehicles. Currently there are no specific therapies preventing or ameliorating the disease course. Although there are new therapeutic modalities in the horizon for D+HUS, present recommended therapy is merely symptomatic. Parenteral volume expansion may counteract the effect of thrombotic process before development of HUS and attenuate renal injury. Use of antibiotics, antimotility agents, narcotics and non-steroidal anti-inflammatory drugs should be avoided during the acute phase. Prevention is best done by preventing primary STEC infection. Underlying aetiology in many cases of aHUS is unknown. A significant number may result from underlying infectious diseases, namely Streptococcus pneumoniae and human immunedeficiency virus. Variety of genetic forms include HUS due to deficiencies of factor H, membrane cofactor protein, Von Willebrand factor-cleaving protease (ADAMTS 13) and intracellular defect in vitamin B12 metabolism. There are cases of aHUS with autosomal recessive and dominant modes of inheritance. Drug-induced aHUS in post-transplantation is due to calcineurin-inhibitors. Systemic lupus erythematosus and catastrophic antiphospholipid syndrome may also present with aHUS. Therapy is directed mainly towards underlying cause.
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PMID:Haemolytic uraemic syndrome: an overview. 1675 34

About one-half of all children with systemic lupus erythematosus have clinical evidence of renal disease at initial presentation, such as proteinuria and acute renal failure. Herein, we report a case of a teenager who presented with end-stage renal disease (ESRD) of uncertain etiology, and who was subsequently determined to have lupus. The purpose of this report is to make health-care professionals aware of this unusual presentation of renal lupus, which has never been reported before. Children presenting in ESRD should be worked-up for autoimmune diseases since the discovery of such a disease process may impact future decision-making, especially with respect to subsequent renal transplantation.
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PMID:End-stage renal disease as the presenting manifestation of renal systemic lupus erythematosus. 1697 72

Several autoimmune diseases are thought to be mediated in part by interleukin (IL)-18. Many are those with associated increased interferon-gamma (IFNgamma) levels such as systemic lupus erythematosus, macrophage activation syndrome, rheumatoid arthritis, Crohn's disease, psoriasis, and graft-versus-host disease. In addition, ischemia, including acute renal failure in human beings, appears to involve IL-18. Animal studies also support the concept that IL-18 is a key player in models of lupus erythematosus, atherosclerosis, graft-versus-host disease, and hepatitis. Unexpectedly, IL-18 plays a role in appetite control and the development of obesity. IL-18 is a member of the IL-1 family; IL-1beta and IL-18 are related closely, and both require the intracellular cysteine protease caspase-1 for biological activity. The IL-18 binding protein, a naturally occurring and specific inhibitor of IL-18, neutralizes IL-18 activities and has been shown to be safe in patients. Other options for reducing IL-18 activities are inhibitors of caspase-1, human monoclonal antibodies to IL-18, soluble IL-18 receptors, and anti-IL-18 receptor monoclonal antibodies.
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PMID:Interleukin-18 and the pathogenesis of inflammatory diseases. 1733 92

Minocycline is a tetracycline derivative with multiple clinical uses including the treatment of various infections, acne vulgaris, and rosacea. Numerous adverse events have been reported ranging from minor complaints such as nausea, to serious life-threatening toxicities such as acute renal failure, hepatotoxicity, and systemic lupus erythematosus. We report the case of an 18-year-old female patient who developed minocycline-induced cutaneous polyarteritis nodosa after taking minocycline for acne vulgaris. The vasculitis resolved after discontinuation of the minocycline without need for corticosteroids. This case is the eighth biopsy-confirmed case of minocycline-induced polyarteritis nodosa. Although minocycline is an effective medication with a wide variety of clinical uses, clinicians must be aware of its potential side effects including autoimmune-related disorders such as polyarteritis nodosa or systemic lupus erythematosus.
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PMID:Minocycline-induced cutaneous polyarteritis nodosa. 1755 82

A 41-year-old Japanese woman with a 25-year history of systemic lupus erythematosus was admitted because of abrupt onset of nephrotic syndrome and acute renal failure. Renal biopsy specimen showed only mild mesangial proliferative glomerulonephritis associated with mesangial deposition of immunoglobulins/complements. No significant immune deposits were found in the glomerular capillary walls, but mild foot process effacement was observed on electron microscopy. Further, two-month corticosteroid therapy improved her massive proteinuria and renal dysfunction, indicating that this patient showed minimal-change nephropathy superimposed on mesangial proliferative lupus nephritis.
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PMID:Emerging minimal-change nephrotic syndrome in a patient with chronic mesangial proliferative lupus nephritis. 1760 39

We assessed the risk factors associated with death in patients hospitalized for juvenile systemic lupus erythematosus (JSLE) and evaluated the autopsy reports. A total of 57,159 hospitalizations occurred in our institution from 1994 to 2003, 169 of them involving 71 patients with JSLE. The most recent hospitalization of these patients was evaluated. Patients were divided into two groups based on mortality during hospitalization: those who survived (N = 53) and those who died (N = 18). The main causes of hospitalization were JSLE activity associated with infection in 52% and isolated JSLE activity in 44%. Univariate analysis showed that a greater risk of death was due to severe sepsis (OR = 17.8, CI = 4.5-70.9), systemic lupus erythematosus disease activity index (SLEDAI) >or=8 (OR = 7.6, CI = 1.1-53.8), general infections (OR = 6.1, CI = 1.5-25), fungal infections (OR = 5.4, CI = 3.2-9), acute renal failure (OR = 5.1, CI = 2.5-10.4), acute thrombocytopenia (OR = 3.9, CI = 1.9-8.4), and bacterial infections (OR = 2.3, CI = 1.2-7.5). Stratified analysis showed that severe sepsis and SLEDAI >or=8 were not confounder variables. In the multivariate analysis, logistic regression showed that the only independent variable in death prediction was severe sepsis (OR = 98, CI = 16.3-586.2). Discordance between clinical diagnosis and autopsy was observed in 6/10 cases. Mortality of hospitalized JSLE patients was associated with severe sepsis. Autopsy was important to determine events not detected or doubtful in dead patients and should always be requested.
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PMID:Risk factors associated with the death of patients hospitalized for juvenile systemic lupus erythematosus. 1765 54

Secondary amyloidosis (AA amyloidosis) has rarely been described in patients with systemic lupus erythematosus (SLE). We, herein, present a 56-year-old female patient, who developed AA amyloidosis following a 22-year history of SLE. She developed severe mitral regurgitation complicated with chordae tendinea rupture that led to acute congestive heart failure and went on a mitral valve replacement, where no flare symptoms of SLE were present. Three months after the operation, she presented with a nephrotic-range proteinuria, acute renal failure, and severe sepsis. She was found to have new vegetations on replaced valve and multi-organ failure caused her death. Re-evaluation of the excised mitral valve revealed AA amyloid deposition. Post-mortem biopsies from the kidney and bone marrow also revealed secondary amyloidosis.
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PMID:AA amyloidosis associated with systemic lupus erythematosus: impact on clinical course and outcome. 1768 56


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