Cases reported "Thrombosis"

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1/176. A giant dissecting aneurysm mimicking serpentine aneurysm angiographically. Case report and review of the literature.

    Intracranial dissecting and giant serpentine aneurysms are rare vascular anomalies. Their precise cause has not yet been completely clarified, and the radiological appearance of such lesions can be different in each case according to the effect of hemodynamic stress on a pathologic vessel wall. For berry aneurysms, available evidence overwhelmingly favors their causation by hemodynamically induced degenerative vascular disease and there is an obvious need to determine the hemodynamic parameters most likely to induce the precursor atrophic lesions. In this study, a case of a giant dissecting aneurysm angiographically mimicking serpentine aneurysm of the right ophthalmic artery is reported and the relevant literature is reviewed to investigate the pathological characteristics and pathogenesis of this lesion. In the present case, radiological investigation of the lesion suggested a serpentine aneurysm, but the diagnosis was corrected to dissecting aneurysm subsequent to the pathological examination of the resected aneurysm. A giant dissecting aneurysm angiographically mimicking serpentine aneurysm and developing as the result of a circumferential dissection located between the internal elastic lamina and media is of particular interest when the etiology of these aneurysms is considered. To our knowledge this is the first report on intracranial dissecting aneurysm mimicking serpentine aneurysm angiographically. Our case illustrates the importance of careful serial section studies for a better understanding of the vascular pathology underlying the processes involved in intracranial serpentine aneurysms. We conclude that serpentine, dissecting and berry aneurysms may all arise by way of similar pathophysiological mechanisms.
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ranking = 1
keywords = vascular disease
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2/176. Thrombotic microangiopathy as a complication of long-term therapy with gemcitabine.

    Three patients with pancreatic carcinoma treated with gemcitabine for 1 year developed clinical and laboratory findings compatible with an indolent form of the hemolytic-uremic syndrome. Renal biopsy specimens in two of these patients showed the characteristic features of thrombotic microangiopathy, and a skin biopsy specimen from the third patient, who presented with livedo reticularis, showed intravascular fibrin deposition. Thrombotic microangiopathy may represent a toxic effect of long-term gemcitabine therapy.
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ranking = 464.63155288311
keywords = microangiopathy
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3/176. FK506-associated thrombotic microangiopathy: report of two cases and review of the literature.

    BACKGROUND: FK506 is a recently developed immunosuppressant that has been useful in improving the survival of transplanted organs. Among the numerous adverse side effects of FK506, thrombotic microangiopathy (TMA) stands out as an infrequent but severe complication. methods: We report two cases of FK506-associated TMA and review the 19 previous reported cases. RESULTS: From these 21 cases, the reported incidence of FK506-associated TMA is between 1% and 4.7%. It is more frequent in females, and the mean age at presentation is 47 years. Eighty-one percent of the cases occurred in patients with kidney allografts, and the remaining patients had liver, heart, or bone marrow transplants. Clinically, TMA was diagnosed at an average interval of 9.3 months from the time of transplantation. patients may be asymptomatic or may present with the full-blown picture of hemolytic uremic syndrome. All patients had an elevated serum creatinine level but did not always show signs of hemolysis. Trough levels of FK506 were not predictive for the development of TMA, but generally a reduction of drug dose correlated with kidney function improvement and disappearance of the hemolytic picture. The renal allograft biopsy provided a conclusive diagnosis in all 17 cases in which this procedure was performed. Treatment, which mainly consisted of reduction or discontinuation of FK506, anticoagulation, and/or plasmapheresis with fresh-frozen plasma exchange, resolved TMA in most patients (57%). However, in one of these patients (5%), the graft was subsequently lost due to causes unrelated to TMA, such as acute or chronic rejection. Despite treatment, one patient (5%) lost the graft due to acute rejection and persistent TMA, and three other patients (14%) who had bone marrow, heart, and liver transplants, died of multiple organ failure, probably unrelated to TMA. In the remaining four patients (19%), response to treatment was not reported. CONCLUSIONS: TMA must be considered in organ transplant patients treated with FK506 whenever kidney function deteriorates, even in the absence of microangiopathic hemolytic anemia. Although TMA usually responds to treatment, it may, in rare cases, lead to loss of kidney function or even the patient's death.
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ranking = 387.19296073592
keywords = microangiopathy
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4/176. Cryosupernatant plasma exchange in the treatment of antiphospholipid antibody syndrome with lupus nephritis.

    We report a case of a 22-year-old female with antiphospholipid antibody syndrome (APS) associated with systemic lupus erythematosus in whom cryosupernatant plasma exchange was effective and improved both the refractory venous thrombosis in her legs and relapsing thrombocytopenia. A renal biopsy specimen showed not only features of active lupus nephritis but also renal arteriolar thrombosis which is considered to be a type of thrombotic microangiopathy (TMA). Because a pathological role of unusually large von willebrand factor (vWF) multimers has been reported in patients with TMA including thrombotic thrombocytopenic purpura, plasma exchange using replacement with cryosupernatant, which is free of unusually large vWF multimers, is likely to be an option of treatment modality for patients with refractory and chronic relapsing APS manifesting TMA.
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ranking = 77.438592147185
keywords = microangiopathy
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5/176. Aortic thrombosis associated with cocaine use: report of two cases.

    cocaine use has been associated with many vascular complications which may involve the carotid, coronary, and renal vascular beds. cocaine may also cause venous thrombosis. This report describes a new entity of cocaine-induced aortic thrombosis. On the basis of clinical findings and response to treatment, a therapeutic algorithm is presented.
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ranking = 17.62723558661
keywords = vascular complication
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6/176. Thrombotic microangiopathy associated with interferon therapy for patients with chronic myelogenous leukemia: coincidence or true side effect?

    BACKGROUND: interferon-alpha (rIFN-alpha) is an established therapy for patients with myeloproliferative disorders. Unusual immune-mediated side effects have been associated with rIFN-alpha therapy. The association of rIFN-alpha therapy with hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) has been reported infrequently. methods: Two patients with chronic myelogenous leukemia (CML) treated with rIFN-alpha-based regimens at the University of texas M. D. Anderson Cancer Center developed thrombotic microangiopathy (HUS/TTP). The course of their disease is described. A third patient who developed renal failure while receiving rIFN-alpha therapy and had no other causative factor for his renal failure is also described. RESULTS: The patients were ages 24, 49, and 36 years, and they had received rIFN-alpha therapy for 37, 67, and 92 months, respectively, prior to the development of the disorder. One patient had discontinued rIFN-alpha 1 month before the event because of presumed rIFN-alpha-related cardiomyopathy. Two patients received hydroxyurea and cytarabine as part of their therapy. No patient was receiving any medication known to be associated with HUS/TTP. None had a history of diarrheal illness, but escherichia coli OH157.H7 was grown from the stool of one patient. Two patients responded to plasmapheresis with normalization of counts and other indices, but both developed renal failure and became dependent on dialysis. One patient had evidence of disease progression and died of multiorgan failure. The third patient required dialysis for 18 months but is currently off dialysis; this patient has some residual renal impairment. CONCLUSIONS: Although no definitive association between rIFN-alpha therapy and thrombotic microangiopathies can be concluded from these data, these and other previously reported cases suggest that HUS/TTP is a rare side effect of rIFN-alpha therapy that should be managed in the standard fashion. Hypotheses regarding the mechanism underlying this association are discussed in this article.
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ranking = 387.19296073592
keywords = microangiopathy
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7/176. The role of early renal biopsy in cyclosporin induced thrombotic microangiopathy.

    Thrombotic microangiopathy is an uncommon complication of cyclosporin immunosuppression following renal transplantation. We present a 15-year-old girl who developed clinical features of acute rejection, but in whom an early biopsy revealed thrombotic microangiopathy, allowing a change to FK506 immunosuppression resulting in excellent graft recovery.
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ranking = 464.63155288311
keywords = microangiopathy
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8/176. Renal involvement of thrombotic thrombocytopenic purpura: special reference to the glomeruloid structures.

    We report the case of a 9-year-old girl with biopsy-proven renal thrombotic microangiopathy in thrombotic thrombocytopenic purpura (TTP), with particular reference to the glomeruloid structures. The renal biopsy sample from this TTP patient revealed platelet thrombus deposition, a glomeruloid structure and aneurysm with relative sparing of the glomeruli. The glomeruloid structure displayed a proliferation of mainly capillary-sized channels lined by factor viii-related, antigen-positive plump endothelial cells embedded in the edematous connective tissue. These glomeruloid vessels communicated with the aneurysmal segment at the end portion of the arteriolar branch. We believe that the glomeruloid structures in TTP represent not merely organization or recanalization of thrombus but rather active angiogenesis through aneurysmal dilation in the arteriolized vessel, probably initiated by platelet agglutination.
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ranking = 77.438592147185
keywords = microangiopathy
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9/176. Thrombotic microangiopathy associated with reactivation of human herpesvirus-6 following high-dose chemotherapy with autologous bone marrow transplantation in young children.

    Thrombotic microangiopathy (TMA) is a serious complication of BMT. Several factors are important in the etiology of TMA, such as cyclosporin A, GVHD, irradiation, intensive conditioning chemotherapy and infection, which cause damage to vascular endothelial cells leading to activation of these cells. We describe two young children with TMA following high-dose chemotherapy with autologous BMT. Development of TMA was accompanied by reactivation of HHV-6, which was identified by both an increase in the copy number of HHV-6 dna in the peripheral blood and a significant increase in antibody titers to HHV-6. Thus, it was suggested that reactivation of HHV-6 together with high-dose chemotherapy played an important role in the pathogenesis of TMA in these patients. Since HHV-6 is known to infect vascular endothelial cells, and CMV which is virologically closely related to HHV-6, has been reported to be a pathogen that causes TMA, infection with HHV-6 of vascular endothelial cells may induce TMA via damage and activation of these cells.
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ranking = 387.19296073592
keywords = microangiopathy
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10/176. Homozygous prothrombin gene mutation and ischemic cerebrovascular disease: a case report.

    We report the case of a 31-year-old woman who, at the age of 26 suffered from an episode of superficial thrombophlebitis in the left leg, experienced two episodes of transient ischemic attacks at the age of 30 and had an ischemic stroke with left-sided hemiparesis at the age of 31 years. A cerebral CT scan showed an ischemic lesion in the right sylvian area involving the opercular and nucleocapsular regions. Her father had had an ischemic stroke at the age of 54 years and died at the age of 58; her mother had had a myocardial infarction at the age of 48 years and died at 51 years from breast cancer. Laboratory investigation of the patient demonstrated high levels of fibrinogen, F II, F VII, F 1 2, FPA and ACA-IgG with low levels of HDL cholesterol associated with homozygosity for the 20210 A genotype. There were no other genetic or acquired prothrombotic defects. In conclusion, this case strongly suggests a clinically significant role ot the prothrombin gene mutation in both arterial and venous thrombosis.
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ranking = 4
keywords = vascular disease
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