Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nodular regenerative hyperplasia (NRH) of the liver is an uncommon pathologic finding associated, in most cases, with rheumatic and hematologic diseases. Although its pathogenesis remains unclear, NRH probably results from liver regeneration to maintain its functional capacity after ischemia-induced injury. An intrahepatic microvascular occlusive mechanism has been considered most likely pathogenetically. NRH may lead to portal hypertension. Thus, the diagnosis of Felty's syndrome must be considered with caution in patients with rheumatoid arthritis (RA) and NRH of the liver. We report seven additional cases of NRH in patients with rheumatic disorders and review the literature to determine the patterns of clinical presentation and natural history of this condition. We also report four patients (three systemic lupus erythematosus [SLE] and one primary antiphospholipid syndrome [PAPS]) in whom antiphospholipid antibodies may have played a role in the genesis of NRH.
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PMID:Nodular regenerative hyperplasia of the liver in rheumatic diseases: report of seven cases and review of the literature. 194 1

A 34-year old woman, with a 3 yr history of severe seropositive rheumatoid arthritis (RA) with lupus anticoagulant and anticardiolipin antibodies, developed a massive anterior myocardial infarction and ischemia of the lower extremities, with disseminated intravascular coagulation resulting from extensive tissue damage. Seven days after admission, she died of severe heart failure complicated by ventricular fibrillation. To our knowledge, this is the first documented case of fatal acute antiphospholipid syndrome in RA.
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PMID:Catastrophic antiphospholipid syndrome with fatal acute course in rheumatoid arthritis. 747 89

The occurrence of lupus anticoagulant and anticardiolipin antibodies was demonstrated in a girl affected by recurrent episodes of visual disturbances, with ophthalmologic evidence of visual impairment and sometimes accompanied by migraine. Systemic lupus erythematosus was excluded on the basis of both clinical and serologic criteria and the diagnosis of primary antiphospholipid syndrome was made. Vascular pathogenesis was suggested by the characteristic symptoms. The serologic demonstration of antiphospholipid antibodies made it possible to relate the illness to an immune-mediated thrombotic tendency. This patient demonstrated that the diagnosis of primary antiphospholipid syndrome must always be considered in focal cerebral or retinal ischemia in childhood.
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PMID:Primary antiphospholipid syndrome and neurologic events. 760 56

The authors describe a healthy young male smoker with familial history of recurrent thromboembolism who presented with severe, rapidly progressive lower limb ischemia and abnormal results from liver function tests. An arteriogram of the lower extremities showed bilateral infrainguinal atherosclerotic arterial occlusions. The laboratory findings, in addition to abnormal liver function findings, included moderately elevated antiphospholipid antibodies and hemostatic abnormalities involving elevated fibrinogen, lipoprotein (a) levels, and deficient fibrinolysis. He underwent bilateral femoral thrombectomy, which was followed by a meticulous anticoagulation, and had gradual improvement of ischemic symptoms and liver functions. This is, to their knowledge, the first reported case in the English literature of premature lower extremity atherosclerosis and antiphospholipid syndrome associated with elevated lipoprotein (a) levels and documented complex hemostatic abnormalities contributing to systemic thrombosis.
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PMID:Massive lower extremity arterial thrombosis and acute hepatic insufficiency in a young adult with premature atherosclerosis associated with hyperlipoprotein(a)emia and antiphospholipid syndrome. A case report. 766 91

We report a case of acute adrenal insufficiency secondary to bilateral adrenal hemorrhage, in a 53 year old patient, occurring in the post-operative course of a lower limb ischemia. The patient was found to have a lupus anticoagulant, and it was concluded that the adrenal insufficiency was related to a primary antiphospholipid syndrome (PAPS). The PAPS is a cause of both, acute and chronic adrenal insufficiency. Endocrinologists are relatively little familiar with this etiology. Pathophysiologically, thrombosis and bilateral adrenal hemorrhage can result in progressive bilateral adrenal atrophy, requiring life long substitution. Therefore, the importance to search for antiphospholipid antibodies in the evaluation of acute and chronic adrenal insufficiency has to be emphasized.
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PMID:[Adrenal insufficiency and antiphospholipid syndrome]. 786 86

We report on eight children who suffered from cerebrovascular ischemia or stroke at the age of 2 or up to 11 years. Antiphospholipid antibodies (APLA) were detected in two cases during the ischemic event and in six cases during follow-up examinations (after six weeks or within a span of six years). In two patients multiple stenoses of basal cerebral arteries were found; one of them suffered from moyamoya syndrome. The acute hemiplegia in one patient was linked to an asymptomatic mycoplasmal infection and APLA. In three cases, one of the parents was also APLA-positive. Seven patients were treated with acetylsalicylic acid, and in four cases immunoglobulin infusions were given. Transient ischemic attacks subsided after the child with the moyamoya syndrome received immunoglobulins. No effect of medication could be established in the other children. The concept of the antiphospholipid syndrome is still evolving. As none of the common risk factors pertaining to strokes in adults apply to children, pediatric research may offer a suitable platform for specific investigations on the causal, pathogenetic role of APLA. We propose that all children suffering from stroke or transient ischemic attacks should be tested for APLA.
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PMID:Antiphospholipid antibodies in cerebrovascular ischemia and stroke in childhood. 820 57

Antiphospholipid antibodies have been reported to occur in ischemic stroke patients, but there have been no previous reports linking these antibodies to spinal cord infarction. A case of spinal cord infarction associated with primary antiphospholipid syndrome in a 6-year-old boy is reported. Magnetic resonance imaging clearly demonstrated marked swelling of the thoracolumbar spinal cord with gadolinium-diethylenetriamine pentaacetic acid enhancement at an acute stage, followed later by cord atrophy. Serological study disclosed positive lupus anticoagulant and immunoglobulin G anticardiolipin antibody. It is suggested that the role of antiphospholipid antibodies as an etiological factor for spinal cord ischemia should be recognized among causes that might have been categorized as either spontaneous spinal cord infarction or myelitis.
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PMID:Spinal cord infarction associated with primary antiphospholipid syndrome in a young child. Case report. 836 Jul 45

The anticardiolipin or antiphospholipid antibody syndrome is characterized by an increased incidence of venous and arterial thromboses. This syndrome may occur in association with systemic lupus erythematosus or independently. Gastroenterological manifestations have included Budd-Chiari syndrome, hepatic infarction, esophageal necrosis with perforation, intestinal ischemia and infarction, pancreatitis, and colonic ulceration. We report a 39-yr-old man with antiphospholipid antibody syndrome complicated by adrenal insufficiency secondary to bilateral adrenal infarction who presented with severe epigastric pain. Endoscopic evaluation disclosed progressive gastric ulceration with necrosis in the distal body. Angiography revealed no vasculitis. Because of intractable pain despite intravenous anticoagulation and narcotic analgesia, the patient was taken to surgery, and an antrectomy with Billroth II gastrojejunostomy was performed. Histological examination revealed widespread vascular occlusive disease involving veins, small arteries, and arterioles present in all layers of the stomach and the perigastric fat consistent with the vasculopathy of the antiphospholipid antibody syndrome. Treatment with high intensity oral anticoagulation and corticosteroids resulted in clinical and endoscopic improvement. This case report extends the gastroenterological manifestations of the antiphospholipid antibody syndrome to include giant gastric ulceration and emphasizes the importance of anticoagulation in treatment.
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PMID:Giant gastric ulceration associated with antiphospholipid antibody syndrome. 912 46

A previously healthy woman presented with ischemic cardiac pain and ST elevation suggestive of acute myocardial infarction following a 45 min argument. Despite receiving tissue plasminogen activator, she developed cardiogenic shock and objective evidence of recurrent ischemia, with only a small creatine kinase rise. Angiography revealed the unexpected findings of normal coronary anatomy and akinesis of the distal two-thirds of the left ventricle. Apart from an iliac vein thrombosis, the remainder of her course was characterized by dramatic recovery of cardiac function. The differential diagnosis of myocardial infarction with angiographically normal coronary arteries is discussed, with emphasis on aspects relevant to this case. The presence of high titre anticentromere antibodies, anticardiolipin antibodies, protein S deficiency and supportive physical findings, suggested the diagnosis of concurrent antiphospholipid antibody syndrome (with secondary acquired protein S deficiency) and CREST syndrome. The pathogenesis likely involved an interaction between stress, vasospasm, and thrombosis.
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PMID:Reversible cardiogenic shock in an angry woman--case report and review of the literature. 868 41

Antiphospholipid antibodies (aPL) have been associated with a variety of neurological disorders, mostly linked to focal neuroparenchymal ischemia or infarction. Cerebral ischemia associated with the antiphospholipid syndrome (APS) occurs at a younger age than typical atherothrombotic cerebrovascular disease, is often recurrent, and high positive GPL values are usually linked to the presence of a lupus anticoagulant. When other features of the syndrome are not present and cerebral ischemia occurs only associated with anticardiolipin immunoreactivity, there appears to be no discerning features of these patients unless GPL > 40 for which recurrent thrombo-occlusive events appear to occur more frequently. Other neurological manifestations associated with aPL include cerebral venous sinus thrombosis, ocular ischemia, dementia, including ischemic encephalopathy, and chorea. The role of aPL in migrainous events is controversial and may not play a role in recent, large case-controlled studies. Most seizures in patients harboring aPL are associated with focal brain infarction.
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PMID:Neurological aspects of antiphospholipid antibody syndrome. 890 59


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