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Query: UMLS:C0002878 (hemolytic anemia)
 7,530 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CSA toxicity includes renal impairment, microangiopathic hemolytic anemia (MAHA), thrombocytopenia (T), and consumptive coagulopathy (CC). We report five BMT patients who developed CSA-associated hematological toxicity. All were conditioned with Ara-C, Cyclophosphamide, Methylprednisolone, TBI, and in two cases busulfan. IV CSA was started the day after marrow infusion and, when practicable, changed to the enteral route. Five patients developed MAHA and T resulting in significantly increased transfusion requirements. All patients had renal impairment and red cell fragmentation. In all patients fragmentation was noted before renal impairment. All developed disproportionate increases in BUN relative to serum creatinine consistent with decreased renal perfusion. Hypertension followed renal impairment in four cases and occurred at the same time as the renal impairment in one case. Two developed CC, prolongation in APTT, and marked decreases in plasma fibrinogen. All patients improved on reduction of the CSA dose. BMT recipients receiving CSA at variable doses may develop evidence of a TTP-like syndrome and/or CC.
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PMID:Coagulation defects in cyclosporine A treated allogeneic bone marrow transplant patients. 304 63

A 45-year-old-woman was presented with fever, microangiopathic hemolytic anemia, thrombocytopenia, purpura, and mental status changes. She was diagnosed as having thrombotic thrombocytopenic purpura (TPP). She was treated with daily plasma exchange and antiplatelet drugs, steroids, and vincristine. This patient had a remarkable course with 18 days of coma on full therapy followed by essentially complete recovery coincident with an increase of the plasma exchange dose to two plasma volumes processed per procedure. The patient has remained well with discontinuation of plasma exchange. We conclude that prolonged coma without evidence of major central nervous system structural lesions in TTP should be treated vigorously and continuously with plasma exchange.
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PMID:Thrombotic thrombocytopenic purpura: prolonged coma with recovery of neurologic function with intensive plasma exchange. 719 46

A 64-year old female had been diagnosed as having thrombotic thrombocytopenic purpura (TTP; Moschcowitz syndrome) in 1984. The initial episode and one recurrence 5 years later were successfully treated with fresh plasma transfusions without plasmapheresis. Two days before the present admission, she noticed pain in the knee and haematomas in both legs. Marked thrombocytopenia (9000/microliters), haemolytic anaemia (lactate dehydrogenase 1800 U/l, haemoglobin 7.8 g/dl, haptoglobin 5 mg/dl) and skin haemorrhages suggested a second recurrence of TTP. The blood film showed a massive increase in fragmented cells (more than 30 per field), microspherocytes and normoblasts. Thrombocyte values initially rose on daily treatment with plasmapheresis using membrane separation and fresh plasma exchange. However, after two attempts at stopping therapy, plasmapheresis and fresh plasma replacement failed to normalise thrombocyte values. The patient had a total of 44 plasmaphereses. Intravenous administration of three doses of 1.5 mg vincristine at intervals of 7 and 5 days combined with further plasmapheresis treatment soon led to normalisation of the thrombocyte count (320,000/microliters), a fall in lactate dehydrogenase (120 U/l) and a disappearance of fragment cells in the blood smear. The patient is still in complete remission 6 months after stopping treatment. Treatment with vincristine should be considered for TTP refractory to treatment.
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PMID:[Treatment of thrombotic thrombocytopenic purpura (Moschcowitz's disease) with vincristine]. 771 34

A 44-year-old women was treated for hyperparathyroidism resulting from parathyroid hyperplasia. Several months later, following a flu-like episode, she developed fever, confusion, abdominal pain, and diffuse petechiae, with severe thrombocytopenia and hemolytic anemia. She died on the 11th day of hospitalization. At autopsy she had multiple endocrine neoplasia type I, with two islet cell tumors, adrenal adenoma, pituitary adenoma, and bronchial carcinoid with liver metastasis. Florid visceral microthrombi involved arterioles and capillaries of the heart, including the conduction system. Brain, kidney, pancreas, adrenal, and portal areas of the liver were also heavily involved, but thrombi were rare in the liver sinusoids and the lungs. PAS-positive subendothelial deposits were demonstrated. In spite of the disseminated malignancy, the morphologic and laboratory findings were inconsistent with disseminated intravascular coagulation (DIC), and supported the clinical diagnosis of TTP. To the best of our knowledge this is the first report association of TTP with MEN and raises the question of a genetic linkage and/or hormonal interaction.
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PMID:Fatal thrombotic thrombocytopenic purpura (TTP) presenting concurrently with metastatic multiple endocrine neoplasia (MEN) type I. 887 34

On June 29, 1995, a 49-year-old man was admitted with acute onset of fever, petechiae on his legs, and mental confusion He had suffered hypertension since 6 months previously and was on nicardipine (60 mg/day), ifenprodil (60 mg/day) and ticlopidine (300 mg/day). He had been on ticlopidine for 4 weeks and on the other drugs for 6 months. Soon after admission he had frequent grand mal seizures and needed mechanical ventilation. A diagnosis of TTP was made. He was treated with plasmapheresis (50 ml/kg per day), aspirin 81 mg/day and dipyridamole 300 mg/day. On the sixth day his mental status returned to normal. He recovered gradually from microangiopathic hemolytic anemia, thrombocytopenia and elevated serum creatinine. We reviewed the literature and discussed the possible mechanism of TTP related to the use of ticlopidine.
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PMID:[Thrombotic thrombocytopenic purpura after administration of ticlopidine]. 896 Jun 74

Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) is a clinical syndrome defined by the presence of thrombocytopenia and microangiopathic hemolytic anemia without a clinically apparent etiology. Patients may also have multiple other symptoms and signs including neurologic and renal abnormalities and fever. In the era prior to effective therapy with plasma exchange, most patients developed multisystem abnormalities and the syndrome was more easily recognized. Now, since there is urgency to begin treatment, sufficient diagnostic criteria for TTP-HUS are only thrombocytopenia and microangiopathic hemolytic anemia without a clinically apparent cause; patients may have no neurologic symptoms, renal abnormalities, or fever. This has lead to an apparent increased incidence because of both the increased importance of early recognition and the decreased specificity of the diagnostic criteria. Effective treatment has also revealed new aspects of the clinical course of TTP-HUS following the initial response to plasma exchange treatment: prompt exacerbations, which are common when plasma exchange is diminished in frequency or discontinued, and later relapses, which may occur many years after the initial episode. This review describes the evolution of the syndrome of TTP-HUS in the current era of effective treatment, and describes the management and clinical outcomes among patients treated by the Oklahoma Blood Institute.
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PMID:Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome: diagnosis and management. 982 22

TTP is a disease with protean manifestations leading to errors in diagnosis. Critical reevaluation of a single observer's experience at LIJMC over a 7-year period is compared to that in published literature. We retrospectively analyzed presentation, clinical course, treatment, and outcome of 15 patients treated for TTP between 1990 and 1997 by one of the authors (V.C.). Minimal diagnostic criteria for TTP were unexplained moderate to severe thrombocytopenia (platelet count <100,000/cmm), microangiopathic hemolytic anemia, with or without low grade fever, and no other attributable etiologies. Neurologic and/or renal dysfunction constituted severe grade. Age range was 5-86 years, with one patient age 5, the youngest yet to date reported with classic TTP. Female to male ratio was 2:1. Overall survival rate was 87%; 40% of patients experienced immediate relapse within the first 4 weeks of presentation; and predisposing causes for immediate relapse appear to be intercurrent infections and severity of presentation. There was a 40% incidence of late relapses of TTP. Two patients with an unusually high number of late recurrences (6 and 16) were HCV-Ab positive and the possible role of persistent HCV infection in recurrent TTP was explored.
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PMID:Thrombotic thrombocytopenia purpura: a single institution experience. 1035 57

The complication of thrombotic thrombocytopenic purpura or hemolytic uremic syndrome (TTP/HUS) can occur in cancer patients. It is characterized by a microangiopathic hemolytic anemia, severe thrombocytopenia, and renal failure. Pulmonary manifestations, especially pulmonary edema, are a common observation. Neurologic changes are also frequently seen. The etiology is unknown at this time. It has been observed in many different types of cancer and is most commonly seen in gastric adenocarcinoma followed by carcinoma of the breast, colon, and small cell lung carcinoma. The hemolysis can be massive and is due to red cell fragmentation, as schistocytes are present in all the cases. Though immune complexes are present in the plasma, the antiglobulin (Coomb's) test is negative. Chemotherapeutic agents, especially mitomycin C, have been implicated as causative factors. There is a correlation of this complication with the cumulative dose. However, chemotherapy cannot account for all the cases as the syndrome can occur in untreated patients. It can be differentiated from disseminated intravascular coagulation by the absence of a coagulopathy. Management should consist of plasma exchange, use of a Staphylococcus aureus column (Prosorba), and control of hypertension. Because of the susceptibility to pulmonary edema, blood volume overloading should be avoided.
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PMID:Thrombotic microangiopathy manifesting as thrombotic thrombocytopenic purpura/hemolytic uremic syndrome in the cancer patient. 1035 89

We present a case of a patient who developed all manifestations of thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) acutely following treatment of cutaneous T-cell lymphoma (CTCL, Sezary syndrome) with deoxycoformycin (pentostatin). Symptoms and signs included severe thrombocytopenia and microangiopathic hemolytic anemia; hallucinations, confusion and disorientation; oliguric acute renal failure requiring hemodialysis; and fever. No other etiology for these symptoms and signs was present. Complete recovery followed treatment for one month with plasma exchange and glucocorticoids. During the succeeding 20 months she has remained well and her CTCL remains stable on no further treatment. This case and two previously published cases suggest that acute and severe TTP-HUS may be a dose-dependent toxicity of deoxycoformycin (pentostatin).
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PMID:Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) following treatment with deoxycoformycin in a patient with cutaneous T-cell lymphoma (Sezary syndrome): A case report. 1044 Sep 15

An increased incidence of TTP has been noted among patients receiving intravascular stents to improve patency in diseased coronary, renal, and peripheral arteries. Placement of transjugular intrahepatic porto-systemic shunt stents is often associated with subsequent development of severe hemolysis. We have prospectively studied the development of microangiopathic hemolysis or TTP in patients undergoing intravascular stent placement for peripheral vascular or renal artery disease. Hemolysis was evaluated both before and after stent placement by measuring complete blood count, total bilirubin, lactate dehydrogenase (LDH), haptoglobin and reticulocyte count, and examining peripheral blood films of all patients. Coagulation parameters, blood urea nitrogen and creatinine were measured to exclude disseminated intravascular coagulation or thrombotic thrombocytopenic purpura as a potential cause of hemolysis. Seventeen patients (median age 69 years) were evaluated. One patient was on ticlopidine. Mean hematocrit fell from 41.8% pre-stenting to 35.5% post-stenting (P = 0.003) but without significant change in reticulocyte count (1.7 vs. 1.6%, P = 0.605), LDH (546 vs. 560 IU/l; P = 0.836), bilirubin (0.62 vs. 0.63 mg/dl; P = 1.0), or haptoglobin (183 vs. 158 mg/dl; P = 0.083). Thus, this drop in hematocrit could not be attributed to hemolysis. Peripheral blood films revealed fewer than 1% schistocytes before and after stent placement in all cases. Absence of significant changes in mean platelet count (240 vs. 210 x 10(9)/L; P = 0.088), fibrinogen (385 vs. 378 mg/dl; P = 0.789), BUN (24.5 vs. 16.8; P = 0.079), and creatinine (1.38 vs. 1.24; P = 0.757) argue against development of TTP or DIC resulting from stent placement. No patient developed new renal impairment, a neurological syndrome, or unexplained fever after stent placement. At a mean of 6 weeks follow-up after stent placement, patients have not developed signs of hemolytic anemia or worsening renal function. Our findings argue against a primary risk of microangiopathic hemolytic anemia or TTP due to intravascular stents in patients not receiving ticlopidine.
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PMID:Intravascular stents do not cause microangiopathic hemolysis or thrombotic microangiopathy. 1054 Mar 68


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