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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An overview is given over etiology and prognosis of cerebral ischemias until the age of 40. In a time period of 19 years, 168 patients were diagnosed with cerebral ischemia until the age of 40 (91 females, 77 males). The most frequent etiology is premature atherosclerosis in patients with vascular risk factors (up to 50%). Cardiogenic embolism is responsible for 1 to 34% of the cases: cardiac valve diseases and endocarditis being the most frequent sources. In 2 to 19% a vasculitis is diagnosed. While infectious arteritis is especially frequent in countries of the third world, immunovasculitides are common in Europe and the USA. Noninflammatory vasculopathies include spontaneous or traumatic dissection, fibromuscular dysplasia and vascular malformations. A migrainous stroke is especially frequent in female smokers with intake of oral contraceptives. During pregnancy both sinus thrombosis and arterial ischemia occur. Hematologic causes for ischemia are polycythemia, thrombocytosis and genetic diseases (sickle cell anemia, AT3-deficiency). Cerebral ischemia may occur in connection with the ingestion of ergot-derivates. The prognosis of cerebral ischemia in young adults is better than in older stroke-patients.
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PMID:[Cerebral ischemia in young adults]. 193 40

Hematologic dysfunction occurs commonly in patients with malignancy. Over half are anemic, often because of acute or chronic blood loss, marrow involvement by the malignancy, marrow suppressive effects of chemotherapy or radiation therapy, or because of the anemia of chronic disease. Less frequently, anemia may result from red cell aplasia, folate or B12 deficiency, hemolytic processes, or hypersplenism. Occasional patients may become polycythemic because of erythropoietin-producing tumors such as renal adenocarcinomas or cerebellar hemangiomas. Elevation of the white cell count is commonly seen, especially in patients with lung cancer. Monocytosis and thrombocytosis, which may be early signs of an underlying malignancy, are also very common and occur in up to half of patients. Thrombocytopenia is commonly a result of therapy or marrow replacement; a few patients may have a syndrome resembling immune thrombocytopenic purpura. Abnormalities of coagulation are present in many patients, and may lead to superficial or deep venous thromboses, pulmonary emboli, nonbacterial thrombotic endocarditis with arterial emboli, bleeding, or acute disseminated intravascular coagulation. A sound understanding of the potential hematologic complications that can result from the malignant process is essential to the clinician caring for cancer patients.
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PMID:Hematologic manifestations of malignancy. 268 Mar 58

The paper is a case report of a 34 year old man with an inferior wall myocardial infarction, episodes of ventricular tachycardia, normal coronary arteries and a large atrial septal defect. Coronary atherosclerosis causes 95% of all myocardial infarcts and 75% in the age group under 35 years. Other possible causes are coronary arteritis, trauma, valuvlopathy, systemic diseases, infective and non-infective endocarditis, polycithemia, thrombocytosis, cocaine abuse. These can be usually excluded by history, physical or laboratory examination. The existence of a large atrial septal defect with dominantly left to right shunting, but occasional right to left shunting, is an indication and a justification for surgical treatment aiming to prevent recurrence by closure of the atrial septal defect. Paradoxical emboli have been recognised in the recent literature as an important cause of cerebral infarction, more rarely of emboli to other locations. The etiology remains difficult to confirm with certitude except when an embolus is seen by echocardiography in transit through a patent foramen ovale. We have also reviewed previously published cases of paradoxical emboli in literature.
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PMID:[Myocardial infarct in a young man with angiographically normal coronary arteries and atrial septal defect]. 1035 29

It has been estimated that up to 10% of hypercoagulable state manifestations in patients with inflammatory bowel disease (IBD) are ischemic strokes. The literature search through MEDLINE and EMBASE highlighted 33 case reports of IBD patients complicated with cerebral arterial infarction during the course of their disease. Most of these patients presented with either left or right sided hemiparesis on admission, while the most common site of arterial infarction was either the right or the left middle cerebral artery. Thrombocytosis and anemia were the most commonly observed potential risk factors for stroke in the laboratory analysis. Other coagulation abnormalities, hereditary thrombotic mutations, hyperhomocysteinemia, hyperlipidemia, structural cardiac abnormalities, endocarditis and cerebral artery vasculitis have also been reported in some of the cases that were reviewed. Even though many of these findings are commonly observed in IBD patients, literature data is still controversial about their causal relationship to ischemic stroke. Similarly, there is also lack of steady evidence and official guidelines for stroke management in both children and adults with IBD comorbidity. Finally, an algorithm based on both the American Heart Association and European Stroke Organization guidelines for stroke management and prevention in the general population, is presented as a reference point for the treatment of IBD patients who are complicated by an ischemic cerebral event.
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PMID:Cerebral arterial infarction in inflammatory bowel diseases. 2402 31

We review the most characteristic clinical and histopathologic findings of the cutaneous manifestations of the occlusive nonvasculitic vasculopathic disorders. Clinically, most of these conditions are characterized by retiform purpura. Histopathologic findings consist of occlusion of the vessel lumina with no vasculitis. Different disorders may produce nonvasculitic occlusive vasculopathy in cutaneous blood and lymphatic vessels, including embolization due to cholesterol and oxalate emboli, cutaneous intravascular metastasis from visceral malignancies, atrial myxomas, intravascular angiosarcoma, intralymphatic histiocytosis, intravascular lymphomas, endocarditis, crystal globulin vasculopathy, hypereosinophilic syndrome, and foreign material. Other times, the occlusive disorder is due to platelet pugging, including heparin necrosis, thrombocytosis secondary to myeloproliferative disorders, paroxysmal nocturnal hemoglobinuria, and thrombotic thrombocytopenic purpura. Occlusive vasculopathy may also appear in cold-related gelling agglutination, like that occurring in cryofibrinogenemia, cryoglobulinemia, cold agglutinin syndrome, and crystalglobulinemia. Microorganisms may also occlude the vessels lumina and this is especially frequent in ecthyma gangrenosum, opportunistic fungi as aspergillosis or fusariosis, Lucio phenomenon of lepromatous leprosy and disseminated strongyloidiasis. Systemic coagulopathies due to defects of C and S proteins, coumarin/warfarin-induced skin necrosis, disseminated intravascular coagulation, and antiphospholipid antibody/lupus anticoagulant syndrome may also result in occlusive nonvasculitic vasculopathy. Finally, vascular coagulopathies such as Sneddon syndrome, livedoid vasculopathy, and atrophic papulosis may also cause occlusion of the vessels of the dermis and/or subcutis. Histopathologic study of occlusive vasculopathic lesions is the first step to achieve an accurate diagnosis, and they should be correlated with clinical history, physical examination, and laboratory findings to reach a final diagnosis.
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PMID:Occlusive Nonvasculitic Vasculopathy. 2775 98