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1/13. Massive myocardial necrosis in thrombotic thrombocytopenic purpura: a case report and review of the literature.

    Thrombotic thrombocytopenic purpura (TTP) is an uncommon syndrome resulting from diffuse occlusion of small arterioles and capillaries by hyaline microthrombi. It is characterized by fever, thrombocytopenic purpura, microangiopathic hemolytic anemia, and neurologic and renal dysfunction. While cardiac pathology in TTP is commonly seen at autopsy, clinical cardiac dysfunction is rare and typically results from conduction system involvement. While 3% to 8% of patients with TTP report chest pain on admission, reports of fatal ventricular pump failure are extremely rare. We now report a case of TTP resulting in death from widespread myocardial necrosis. This patient presented with elevated cardiac enzymes and electrocardiographic disturbances that mimicked viral myocarditis, as well as a profound thrombocytopenia. Such a case may represent the extreme of a distribution of cardiac involvement in TTP or the consequence of an unidentified autoimmune process capable of precipitating severe myocardial TTP.
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2/13. Thrombotic thrombocytopenic purpura: a syndrome of intravascular platelet consumption.

    In four of five patients with thrombotic thrombocytopenic purpura (TTP) in whom serial tests of hemostatic function were performed, severe thrombocytopenia, normal plasma fibrinogen concentrations and mildly increased concentrations of fibrinogen/fibrin degradation products were observed. Widespread platelet thrombi were found in arterioles and capillaries. Fibrin could be seen around some of the platelet clumps and was the main component in a small number of the thrombi in two patients. The observations show that TTP is a disorder in which intravascular platelet consumption results in disseminated platelet thrombosis. The coagulation system is apparently activated secondarily to platelet aggregation and variable quantities of fibrin are incorporated into the thrombi. Clinical improvement resulted from combined therapy with corticosteroids, heparin and drugs that suppress platelet function.
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3/13. Thrombotic thrombocytopenic purpura associated with a prolactin-producing pituitary adenoma.

    We report here the case of a 44-year-old woman with thrombocytopenia, anemia, convulsions, hyperprolactinemia, and galactorrhea. The patient died of cardiac failure. autopsy revealed PAS-positive and von willebrand factor-positive microthrombi in the arterioles and capillaries of many organs, mainly in the heart and brain, confirming the clinical diagnosis of thrombotic thrombocytopenic purpura. In the pituitary, a prolactin-producing adenoma was identified. To our knowledge, thrombotic thrombocytopenic purpura accompanied by a prolactin-secreting pituitary adenoma has not yet been described. The question of whether the association between the vascular changes and the pituitary adenoma is incidental or causal cannot be answered. Further studies are required to determine whether prolactin released from the pituitary tumor in excess played a role in the formation of microthrombi causing multiple organ failure and the demise of the patient.
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4/13. Thrombotic thrombocytopenic purpura as a complicating factor in a case of polymyositis and sjogren's syndrome.

    A 62-year-old woman was admitted for evaluation of muscular weakness, skin pigmentation, dry mouth, and interstitial pneumonia. During the course of her stay, adult respiratory distress syndrome, hemolytic anemia, renal failure, neurologic dysfunction, and thrombocytopenia appeared. A clinical diagnosis of thrombotic thrombocytopenic purpura (TTP) accompanied by polymyositis and sjogren's syndrome was made. She died two weeks after the beginning of plasmapheresis, and an autopsy was performed. immunohistochemistry disclosed deposits of IgM, fibrinogen, and C1q in glomeruli and arterioles and deposits of C3 in small arteries. von Willebrand's factor antigen, which promotes the adhesion of platelets to the subendothelium, was positive in onion-peeled arteries of the kidney and the spleen. These results suggest that immune complexes may have triggered a sequence of events from vascular endothelial injury to TTP.
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5/13. Thrombotic thrombocytopenic purpura: report of case.

    TTP is an acute, usually fatal disease of unknown etiology. Diagnostic confirmation of the disease requires histologic demonstration of the deposition of hyaline thrombi within the lumens of arterioles and capillaries in the absence of vasculitis. The clinical, laboratory, and histological manifestations of TTP were reviewed and a case was reported in which a gingival biopsy specimen was used to confirm the diagnosis. Emphasis is placed on the rapidity and ease of gingival biopsy and the possibility of earlier institution of therapy.
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6/13. Thrombotic thrombocytopenic purpura with C'3 vascular deposits: report of a case.

    A case of thrombotic thrombocytopenic purpura in a young woman in which platelet microthrombi were distributed in small vessels throughout the body is reported. IgM and complement (C'3) were demonstrated in capillary and small arteriole walls by immunofluorescent microscopy. These findings support the findings of a previous case report, and are further evidence for a possible primary immune etiology for thrombotic thrombocytopenic purpura.
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7/13. Thrombotic thrombocytopenic purpura in a child with Alexander's disease.

    Thrombocytopenic purpura developed in a 14-year-old boy with Alexander's disease; he died. The proximity of Rosenthal fibers to small vessels in the brain, the presence of perivascular lymphocytes in the brain, and the presence of complement in renal arterioles suggest that the Rosenthal fibers could have injured the endothelium-basement membrane resulting in an immune response triggering the thrombotic thrombocytopenic purpura.
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8/13. Comparative immunopathologic studies of thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome and disseminated intravascular coagulation.

    The vascular lesion of thrombotic thrombocytopenic purpura was characterized by two distinct types of changes in the arteriole of the heart and brain: (1) multiple incomplete vascular occlusions due to the subendothelial deposits composed of a homogeneous fibrin fibrinogen-like substance and platelets without the formation of polymerized fibrin; (2) vascular wall thickening due to the intramural granular deposits of IGM and beta 1C. A patient with hemolytic-uremic syndrome 9 days after the onset of the disease, exhibited (1) the formation of fibrin-thrombi in the glomerular capillary lumens, and (2) the granular deposits of IgM and beta 1C along the glomerular capillary walls and in the mesangium. In contrast, the case in which the symptoms subsided five weeks after the onset exhibited neither fibrin-thrombus formation nor the deposits of IgM and beta 1C in the glomeruli. The vascular lesions of disseminated intravascular coagulation accompanied by pancreas carcinoma was located mainly in the capillaries, and were characterized by the formation of numerous fibrin-thrombi. Although the glomeruli contained numerous thrombi, there was neither endocapillary proliferation nor deposits of immunoglobulins and complement components.
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9/13. Hemolytic uremic syndrome complicating postinfectious glomerulonephritis in the adult.

    Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura is known to occur as a secondary complication of primary renal diseases, specifically of lupus nephritis, membranous glomerulonephritis, and focal segmental glomerulosclerosis. In a patient without a family history of hemolytic uremic syndrome/thrombotic thrombocytopenic purpura we observed biopsy-confirmed postinfectious glomerulonephritis with humps, with simultaneous subendothelial hyaline deposits and fibrinoid thrombi in arterioles. The patient had a history of febrile pharyngitis with diarrhea 10 days prior to renal biopsy. He presented with transient elevation of serum creatinine, a nephritic sediment, and hypertension not exceeding 160/100 mm Hg. The patient also had purpura, transient thrombocytopenia, and signs of intravascular hemolysis. Results of verocytotoxin serology were negative. With the exception of isolated microhematuria, all findings reverted to normal within 8 weeks without any specific treatment. This case illustrates that hemolytic uremic syndrome/thrombotic thrombocytopenic purpura may complicate primary postinfectious glomerulonephritis in adults.
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10/13. Thrombotic thrombocytopenic purpura: the challenges of a complex disease process.

    Thrombotic thrombocytopenic purpura is an acute, rare disorder with a poor prognosis, though the survival rate has improved dramatically in the past 20 years. It is a complex disease characterized by thrombocytopenia, hemolytic anemia, fluctuating neurologic symptoms, fever, and renal dysfunction. The incidence of thrombotic thrombocytopenic purpura appears to be increasing in frequency, with women affected twice as often as men. The median age of onset is in the fourth decade of life. The clinical manifestations of thrombotic thrombocytopenic purpura are caused by widespread deposition of platelet microthrombi that occlude the capillaries and arterioles, especially evident in the brain, kidney, and bone marrow. The resulting intravascular platelet consumption is responsible for bleeding and petechiae. The etiology is unknown, but may be caused by immune system mediated damage to the endothelium. The complexity of this disease challenges the health care team and demands highly skilled medical and nursing management. This article presents a summary of the history and pathophysiology of the disease, clinical course with case study, medical treatment, nursing diagnoses and interventions, and conclusions.
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