Disease relevance of Plasmapheresis

• Treatment with plasmapheresis plus a standard regimen of prednisone and cyclophosphamide therapy does not improve the clinical outcome in patients with systemic lupus erythematosus and severe nephritis, as compared with the standard regimen alone [1].
• Epoprostenol and plasmapheresis in complicated HELLP syndrome with pancreatitis [2].
• Parvovirus B19-induced red cell aplasia treated with plasmapheresis and immunoglobulin [3].
• Evidence is provided that other immunosuppressants (azathioprine, cyclophosphamide, poly-ICLC) and possibly plasmapheresis, alone or in conjunction with corticosteroids, may have a beneficial role in controlling difficult cases of chronic relapsing polyneuropathy [4].
• Five patients with Eaton-Lambert syndrome (ELS) without associated malignancy were first treated by plasmapheresis alone, and subsequently by plasmapheresis combined with prednisone and azathioprine therapy [5].

Psychiatry related information on Plasmapheresis

• PANDAS with catatonia: a case report. Therapeutic response to lorazepam and plasmapheresis [6].

High impact information on Plasmapheresis

• Plasma antithrombin III and plasminogen levels in chronic plasmapheresis [7].
• Reduction of plasma cholesterol concentration over 2 h by plasmapheresis increased reductase activity, the degree of which was directly proportional to the LDL-receptor status of the subjects [8].
• In addition, rapid depletion of circulating cholesterol levels by plasmapheresis led to an approximately twofold elevation in enzyme activity within 90 min of treatment [9].
• 8 patients with severe disease and histamine-releasing activity in their sera underwent plasmapheresis [10].
• The hypoglycaemia did not respond to plasmapheresis or azathioprine alone, but it remitted after the addition of prednisolone, and the erythrocyte receptor binding of insulin became normal [11].

Chemical compound and disease context of Plasmapheresis

• Hypersensitivity reaction to bacillus Calmette-Guérin treated with plasmapheresis [12].
• The development of metabolic alkalosis during plasmapheresis can be explained by the large sodium citrate load given during the procedure [13].
• We present six patients with acute fulminant episodes of CNS inflammatory demyelination who responded to therapeutic plasmapheresis after failing a course of high-dose methylprednisolone administered IV [14].
• Phenytoin removal by plasmapheresis in thrombotic thrombocytopenic purpura [15].
• Improvement followed treatment with dexamethasone, cyclophosphamide, and plasmapheresis, but he died of pulmonary embolism [16].

Biological context of Plasmapheresis

• We also found, although in uncontrolled trials, that treatment with either prednisone or plasmapheresis was followed by clinical improvement; since plasmapheresis is not likely to further depress cell-mediated immunity, we suggest that it be the initial therapy [17].
• Serum inhibitors of hematopoiesis in a patient with aplastic anemia and systemic lupus erythematosus. Recovery after exchange plasmapheresis [18].
• Improved hormone bioavailability was further evidenced by the reduction in the hypoglycemic delay after i.v. insulin from 90 min before any treatment to 60 min after plasmapheresis and 30 min after steroid administration [19].
• Following acute reduction of plasma cholesterol by plasmapheresis, the quantitative increases in beta-VLDL cholesterol concentrations (210 to 364 mg/dl) over the subsequent 24 hr were in agreement with the rise calculated from the plasma clearance kinetics of 125I-labeled beta-VLDL (378 mg/dl per 24 hr) [20].
• The patient recovered without lasting sequelae following reduction of increased intracranial pressure by mannitol, hyperventilation, and phenobarbital and prolonged immunosuppression by plasmapheresis, steroids, and cyclophosphamide [21].

Anatomical context of Plasmapheresis

• The patient was treated wtih cyclophosphamide, steroids, factor VIII concentrates, and repeated plasmapheresis (including three times with NCI-IBM blood-cell separator) [22].
• We conclude that (1) plasmapheresis has only transient effects on islet-cytotoxic antibody levels in children with IDDM; (2) these antibodies decrease in most, but not all, subjects over the first 18 mo after diagnosis; and (3) the level of cytotoxic antibodies in IDDM plasma at diagnosis has no predictive effect on residual B-cell function [23].
• We determined the effects of plasmapheresis on cytotoxic antibodies to islet cells in 10 children (aged 11-16 yr) with newly diagnosed insulin-dependent diabetes mellitus (IDDM), as well as the plasma levels of antibodies over the next 30 mo and their relation to serum C-peptide concentrations [23].
• (2) The second group aims to restore the defective immune system; it includes thymosin (thymopentin), interleukin-2, cyclosporine, plasmapheresis, bone marrow transplantation, inosine, sodium diethyldithiocarbamate, methionine-enkephalin and carrisyn [24].
• High levels of ABO isoagglutinins prior to plasmapheresis and rapidly rising titers posttransplantation may have predicted bone marrow graft rejection in this patient [25].

Associations of Plasmapheresis with chemical compounds

• Plasmapheresis and Factor VIIIC inhibitors [26].
• D-Penicillamine-induced Goodpasture's-like syndrome in primary biliary cirrhosis--successful treatment with plasmapheresis and immunosuppressives [27].
• Plasmapheresis appears not to enhance the effectiveness of prednisone and daily oral cyclophosphamide [28].
• Pharmacologic treatment with almitrine bismesylate, somatostatin analog, and indomethacin and treatment with plasmapheresis have been disappointing [29].
• Initial therapeutic trials of prednisone (100 mg daily for 4 to 6 months) and plasmapheresis were unsuccessful [30].

Gene context of Plasmapheresis

• Acute plasmapheresis in 11 of the 13 patients significantly increased the plasma clearance of TNF-alpha (P = .02) [31].
• Based on these data, we would suggest a therapeutic approach in selected patients that includes the removal of serum inhibitory factors by plasmapheresis and restoration of cellular defects by combined IL-2 with or without INF-alpha [32].
• Some reports have shown that patients with a very low plasma level of ADAMTS13 respond very well to plasmapheresis [33].
• In the present study, a rapid and comprehensive method is presented to analyze IGFBPs and IGFBP fragments in the plasma of a child with acute renal failure (ARF) who had undergone plasmapheresis [34].
• The protein A immunoadsorption column is a medical device that in conjunction with plasmapheresis can be used in patients with refractory RA [35].

Analytical, diagnostic and therapeutic context of Plasmapheresis

• Twenty-six patients with rheumatoid arthritis (average age, 57 years; average duration of disease, 11 years) who were unresponsive to antiinflammatory and slow-acting antirheumatic drug therapy were entered into a controlled, double-blind, crossover study to assess the efficacy of plasmapheresis therapy [36].
• Further investigation in 4 of the patients showed significantly reduced skin-test responses to fresh post-exchange autologous sera after plasmapheresis compared with stored pre-exchange sera, but the response to intradermal histamine remained unchanged [10].
• Diazepam was minimally beneficial, but after treatment with plasmapheresis and corticosteroids, she was still asymptomatic when seen 5 years later [37].
• To investigate the effect of an intensified treatment protocol synchronizing plasmapheresis with subsequent pulse cyclophosphamide for severe systemic lupus erythematosus (SLE) [38].
• At diagnosis, treatment was initiated immediately with prednisone (80 mg/day) and plasmapheresis, which was performed as a first-aid measure [39].

References