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Plasma Exchange Therapy (plasma + exchange_therapy)
Selected AbstractsOutcome of Plasma Exchange Therapy in Thrombotic Microangiopathy After Renal TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 10 2003Vanji Karthikeyan Thrombotic microangiopathy (TMA) in renal transplant recipients is commonly associated with calcineurin inhibitors (CNIs), though several factors such as vascular rejection, viral infections and other drugs may play a contributory role. We report a series of 29 patients with TMA, all of whom were on CNIs. Though plasma exchange (PEx) is widely used to treat TMA, therapeutic guidelines are not well defined. All our patients were treated with PEx and discontinuation of CNIs. Thrombotic microangiopathy was diagnosed at a median of 7 days post-transplant. The mean decrease in Hgb and platelets during TMA was 66% and 64%, respectively, and peak serum creatinine during TMA was 7.4 ± 2.9 mg%. Mean duration of PEx therapy was 8.5 (range 5,23) days. Recovery of platelet count to 150K/mcL and Hgb to 8,10 g/dL were used as endpoints for PEx. Twenty-three/29 (80%) patients recovered graft function after PEx. Twenty/23 (87%) patients who recovered were placed back on CNl. Nineteen/20 (95%) patients tolerated reinstitution of CNl without recurrence of TMA. In post-transplant TMA, PEx was associated with a graft salvage rate of 80%, reversal of hematological changes can be used as the endpoint for PEx therapy and CNl can be reintroduced without risk of recurrence in the majority of patients. [source] Alpha-1-antitrypsin deficiency associated with panniculitis treated with plasma exchange therapyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 9 2004Priscila De Oliveira MD Background, Alpha-1-antitrypsin is the principal serum protease inhibitor. In addition to the well-recognized association with early-onset emphysema and cirrhosis, alpha-1-antitrypsin deficiency may be associated with panniculitis. The treatment of this type of panniculitis presents a significant challenge. Previous attempts using immunosuppressive, anti-inflammatory, and cytotoxic drugs have shown variable results. Aim, To report a case of alpha-1-antitrypsin deficiency-associated panniculitis treated with plasma exchange therapy. Methods, A 23-year-old patient developed painful red nodules on her thighs and buttocks with spontaneous ulceration and discharge of oily fluid. A skin biopsy specimen showed septal and lobular panniculitis. The serum alpha-1-antitrypsin level was 22 mg/dL. She was treated with plasma exchange therapy. Results, Treatment of this patient with plasma exchange therapy led to the control of the cutaneous lesions. Conclusions, Plasma exchange therapy represents an alternative treatment which restores serum and tissue alpha-1-antitrypsin levels. This method is proposed because of its clinical benefits and greater availability. [source] Plasma exchange therapy for victims of envenomation: is this reasonable?JOURNAL OF CLINICAL APHERESIS, Issue 4 2006Liron Pantanowitz First page of article [source] Plasma exchange therapy in rapidly progressive glomerulonephritisNEPHROLOGY, Issue 3 2001Bruce A Pussell No abstract is available for this article. [source] Alpha-1-antitrypsin deficiency associated with panniculitis treated with plasma exchange therapyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 9 2004Priscila De Oliveira MD Background, Alpha-1-antitrypsin is the principal serum protease inhibitor. In addition to the well-recognized association with early-onset emphysema and cirrhosis, alpha-1-antitrypsin deficiency may be associated with panniculitis. The treatment of this type of panniculitis presents a significant challenge. Previous attempts using immunosuppressive, anti-inflammatory, and cytotoxic drugs have shown variable results. Aim, To report a case of alpha-1-antitrypsin deficiency-associated panniculitis treated with plasma exchange therapy. Methods, A 23-year-old patient developed painful red nodules on her thighs and buttocks with spontaneous ulceration and discharge of oily fluid. A skin biopsy specimen showed septal and lobular panniculitis. The serum alpha-1-antitrypsin level was 22 mg/dL. She was treated with plasma exchange therapy. Results, Treatment of this patient with plasma exchange therapy led to the control of the cutaneous lesions. Conclusions, Plasma exchange therapy represents an alternative treatment which restores serum and tissue alpha-1-antitrypsin levels. This method is proposed because of its clinical benefits and greater availability. [source] Excellent response of refractory life-threatening thrombotic thrombocytopenic purpura to cyclosporine treatmentINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 1 2004M. Itälä Summary The introduction of plasma exchange has significantly improved the outcome of thrombotic thrombocytopenic purpura (TTP), and survival has increased from 10 to 80,90%. TTP refractory to plasma exchange therapy, however, is still a therapeutic challenge. We describe here a patient who partially responded to plasma exchange therapy, but remained totally dependent on plasma infusions. Several attempts to discontinue plasma therapy repeatedly lead to relapses. TTP did not response to vincristine, either. After 3 months treatment with plasma therapy, cyclosporine was started. Plasma therapy could be discontinued after 3 weeks on cyclosporine, and serum LDH and blood platelet count were gradually normalized during 2 months. Cyclosporine was tapered off after 6 months treatment, and the patient has stayed in remission ever since. We conclude that cyclosporine is a worthwhile treatment option in patients with refractory TTP. [source] Homozygous familial hypercholesterolemia: Long term clinical course and plasma exchange therapy for two individual patients and review of the literatureJOURNAL OF CLINICAL APHERESIS, Issue 6 2009Roy Beigel Abstract Familial hypercholesterolemia (FH) is an autosomal dominant disease. Homozygous FH (HFH) manifests with severe hypercholesterolemia since birth (cholesterol levels >5,6 the upper normal limit), which, if untreated, leads to early onset accelerated atherosclerosis and premature coronary death, usually before the 2nd or 3rd decades of life. Various invasive procedures (iliocecal bypass, porto-caval shunt, liver transplant, and gene therapy) have been introduced for lowering low density lipoprotein (LDL) aiming at reducing atherosclerosis and improving survival of HFH patients. Of all the various methods, LDL apheresis has become the most attractive. Although its impressive effect on LDL-C reduction is well established, its long-term (of more than 10 year) effect on the atherosclerotic process and specifically cardiac end-points in HFH is hardly documented. We herewith report on the longest term lipophoresis so far reported in two HFH patients, each treated with plasma-exchange and LDL-apheresis for more than 20 years. The observations provide an opportunity to focus on various aspects regarding not only the procedure itself but also its effect on various clinical endpoints. By this description together with reviewing the literature, we discuss several issues, some of them are generalized while others are individualized, dealing with the approach of long term LDL apheresis in HFH. J. Clin. Apheresis 2009. © 2009 Wiley-Liss, Inc. [source] Atypical presentations of thrombotic thrombocytopenic purpura: A review,JOURNAL OF CLINICAL APHERESIS, Issue 1 2009Ravi Sarode Abstract Thrombotic thrombocytopenic purpura (TTP) is diagnosed by the presence of microangiopathic hemolytic anemia and thrombocytopenia in a patient who frequently presents with central nervous system involvement and, to a lesser extent, renal dysfunction. Recent understanding of the pathophysiology of TTP due to severe deficiency of von Willebrand factor cleaving protease, known as ADAMTS13, has improved diagnosis of TTP. Once the diagnosis is suspected, life-saving therapeutic plasma exchange therapy is initiated. Occasionally, an unusual clinical presentation makes TTP diagnosis difficult, thus resulting in a delay in the management of TTP. This review highlights a variety of atypical TTP presentations described in the literature. It is intended to bring unusual scenarios to the clinician's awareness, so that timely treatment can be delivered. J. Clin. Apheresis, 2009. © 2008 Wiley-Liss, Inc. [source] Rituximab therapy for thrombotic thrombocytopenic purpura: A proposed study of the Transfusion Medicine/Hemostasis Clinical Trials Network with a systematic review of rituximab therapy for immune-mediated disordersJOURNAL OF CLINICAL APHERESIS, Issue 1 2006James N. George Abstract The rationale for immunosuppressive therapy of thrombotic thrombocytopenic purpura (TTP) was established by observations that TTP may be caused by autoantibodies to ADAMTS13. Patients with high-titer autoantibodies to ADAMTS13 may have a higher mortality, and survivors may require prolonged plasma exchange therapy in spite of adjunctive glucocorticoid treatment. More intensive immunosuppressive therapy with rituximab may provide benefit for many of these patients. The Transfusion Medicine/Hemostasis Clinical Trials Network is developing a randomized, clinical trial to test the hypothesis that addition of rituximab to standard treatment of TTP with plasma exchange and glucocorticoids will decrease initial treatment failure rates as well as subsequent relapses over the following 3 years. To provide the background data for this clinical trial, a systematic review of all published reports on rituximab treatment of immune-mediated disorders was performed. Twelve articles have reported 27 patients treated with rituximab for TTP, with benefit described in 25 (93%) of the patients. Additional reports have described rituximab treatment of 37 other immune-mediated disorders, with clinical response in most patients. These observations from small uncontrolled case series provide the background and rationale for a randomized clinical trial to establish the role of rituximab in the management of patients with TTP. J. Clin. Apheresis. 21: 49,56, 2006 © 2006 Wiley-Liss, Inc. [source] Role of splenectomy in patients with refractory or relapsed thrombotic thrombocytopenic purpuraJOURNAL OF CLINICAL APHERESIS, Issue 2 2003Nicole A. Aqui Abstract Thrombotic thrombocytopenic purpura (TTP) was once uniformly fatal. Therapeutic plasma exchange in combination with immunosuppressive and anti-platelet agents, however, have resulted in improved survival rates of greater than 80% for patients with TTP. In spite of aggressive plasma exchange and adjuvant therapy, a number of TTP patients are refractory to treatment. In addition, up to 40% of TTP patients who initially respond to therapy eventually relapse. Alternative therapies such as splenectomy have been used with varying degrees of success in refractory and relapsing TTP patients. The usefulness of splenectomy in preventing relapse of TTP or treating those patients who are refractory to plasma exchange remains controversial. We present a single institution's experience with 14 patients who underwent splenectomy for refractory (six patients) or relapsed (eight patients) TTP since 1984. In both patient groups, splenectomy induced stable long-term remissions. Six of six (100%) patients who were refractory to plasma exchange, survived to be discharged from the hospital, apparently free of disease. Four of eight patients (50%) who had a splenectomy for relapsing TTP went into a complete remission and had no further relapses of their disease. Moreover, in relapsing patients who failed to experience long-term remission, the relapse rate after splenectomy was 0.3 events per patient year compared to 1.0 events per patient year prior to splenectomy. We conclude that splenectomy is a reasonable treatment option for TTP patients refractory to standard plasma exchange therapy or who have experienced multiple and/or complicated relapses. We believe this is the first series that demonstrates efficacy of splenectomy in plasma exchange-refractory TTP. J. Clin. Apheresis 18:51,54, 2003. © 2003 Wiley-Liss, Inc. [source] Successful Renal Transplantation in Factor H Autoantibody Associated HUS with CFHR1 and 3 Deficiency and CFH Variant G2850TAMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2010A. M. Waters Factor H (CFH) autoantibodies are associated with atypical hemolytic uremic syndrome (aHUS). Peritransplantation plasma exchange therapy and intensification of immunosuppression, with adjuvant use of anti-CD20 monoclonal antibodies has recently been advocated for cases of CFH-autoantibody associated aHUS. In this report, we describe successful deceased donor renal transplantation in a case of CFH-autoantibody associated aHUS with combined CFHR1 and 3 deficiency in addition to the CFH sequence variant, (cG2850T, pGln950His). CFH-autoantibodies were detected 2 weeks prior to transplantation. Disease recurrence was not observed using basiliximab, an IL2-receptor antagonist and high-dose corticosteroids with mycophenolate mofetil. Adjuvant therapies such as Rituximab nor intensification of plasma therapy were employed. Consequently, careful consideration needs to be given to the use of additional immunosuppression in certain cases of CFH-autoantibody associated aHUS. Serial measurement of CFH-autoantibodies is required in the immediate pre- and posttransplantation period to further clarify their role as a factor in the recurrence of aHUS posttransplantation. Furthermore, delineation of the functional significance of CFH-autoantibodies is warranted in individual cases. [source] Diagnosis of thrombotic thrombocytopenic purpura based on modulation by patient plasma of normal platelet adhesion under flow conditionBRITISH JOURNAL OF HAEMATOLOGY, Issue 4 2003Boris Shenkman Summary. We have designed a simple test for the early diagnosis and treatment monitoring of thrombotic thrombocytopenic purpura (TTP). We examined plasma from 24 TTP patients and normal plasma using a cone and plate(let) analyser (CPA). Test plasma was mixed with citrated normal whole blood (group O) and subjected to flow at a shear rate of 1800/s. Mixing normal plasma (12·5, 25, 50 or 75 µl) with heterologous normal whole blood (final volume of 200 µl) resulted in a decrease of surface coverage (SC, maximally by 63%) and, to a lesser extent, of average size (AS, maximally by 37%) due to dilution of the blood sample. In contrast, mixing the same quantities of acute TTP plasma with normal blood yielded an increase in both SC (up to 125%) and AS (up to 130%). Increased SC and/or AS were detected in all 15 patients in acute phase and in three out of 14 patients in remission. Following repeated plasmapheresis, the enhanced platelet deposition in five patients with acute TTP returned to almost normal patterns. Mixing plasma from patients with other thrombocytopenic conditions in this way resulted in a decrease in both SC and AS, and did not differ from control subjects. In conclusion, the CPA is a simple and specific laboratory test that can be used for the diagnosis and monitoring of plasma exchange therapy in TTP. [source] | ||||||||||