Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 62-year-old woman was admitted to our hospital because of general malaise in May, 1987. No hepatosplenomegary, skin eruption or lymphadenopathy was detected. Laboratory examinations showed mild anemia, thrombocytopenia, normal leukocyte count with no lymphocyte abnormality, hypogranular neutrophils, elevated serum lactic dehydrogenase, increased C-reactive protein and hypoxia. Bone marrow aspirate was normocellular with dysplastic changes in erythroid and megakaryocytic lines which agree with a diagnosis of myelodysplastic syndrome (MDS). She was treated with prednisolone which relieved her symptom but she developed high fever, hemiplegia and disturbance of consciousness and died in August, 1987. Necropsy of the kidney revealed large mononuclear cells within the lumen of small blood vessels. Immunohistochemical study of these malignant cells showed positive reaction to the anti-LCA and anti-L26 antibodies. And electron microscopy showed no azure granules in these cells. Then we diagnosed as neoplastic angioendotheliosis (NAE). To our knowledge, this is the first report of NAE with abnormalities in myeloid, erythroid and megakaryocytic lineages. These results suggest that NAE with MDS originate from a multipotent stem cell.
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PMID:[Myelodysplastic syndrome with neoplastic angioendotheliosis: report of a case]. 175 62

The authors report 23 cases of heparin-induced thrombocytopenia with vascular complications. The clinical presentation consisted of arterial ischaemia in 16 cases, hemiplegia in 1 case, 4 cases of blue thrombophlebitis, 1 case of bilateral thrombophlebitis, 1 case of pulmonary embolism. The vascular surgeon faced with such emergency complications must be aware of the difficulties of clinical (atypical forms) and laboratory diagnosis (unreliability of platelet aggregability tests). Arterial occlusions are generally accessible to treatment with a Fogarty catheter during an operation performed without the use of heparin. The excessively frequent delay in diagnosis explains the severity of these complications and 2 deaths, 1 case of paraplegia, 4 cases of amputation secondary to arterial occlusion, 4 cases of severe postphlebitis disease, including 2 cases requiring transmetatarsal amputation and one case of pulmonary sequelae after pulmonary embolism were observed in our series of 23 patients. The diagnosis of heparin-induced thrombocytopenia requires immediate discontinuation of heparin therapy. Replacement by low molecular weight heparin is not devoid or risks and can only be considered with a negative platelet aggregability test (in the presence of low molecular weight heparin). As these test can be rarely performed as an emergency procedure, the use of rapid-acting oral anticoagulants appears to be the most reliable solution. The place of platelet antiaggregants and partial interruption of the inferior vena cava is discussed.
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PMID:[Heparin-induced thrombocytopenia. Practical management of vascular complications]. 176 34

The authors report 21 cases of heparin-induced thrombocytopenia with ischemic vascular complications. The clinical presentations were peripheral arterial ischemia (16 cases), hemiplegia (1 case) and deep vein thrombosis (4 cases). The vascular surgeon confronted by these complications in an emergency situation should recognise the difficulties of clinical diagnosis (atypical forms) and biological investigations (problems of tests of platelet aggregation). Arterial occlusions are usually accessible to disobliteration with a Fogarty catheter without peroperative heparinisation. Delayed diagnosis explains the seriousness of these complications; in our series of 21 patients, there were 2 deaths, 1 paraplegia, 4 amputations due to arterial problems, 4 severe post-deep vein thrombosis conditions, two of which followed trans-metatarsal amputation. The diagnosis of heparin-induced thrombocytopenia implies immediate withdrawal of heparin therapy. A relay with a low molecular weight heparin is not without risk and should only be undertaken after a negative platelet aggregation test (with the low molecular weight heparin). These tests are rarely practicable in emergency situations and a relay using oral anti-vitamin K antagonists with a rapid onset of action is probably the safest option.
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PMID:[Ischemic vascular complications following thrombopenia induced by heparin. Diagnostic and therapeutic problems]. 212 62

Pentosan polysulfate may induce severe thrombocytopenia by an immunoallergic mechanism similar to that observed with heparin. We report five cases of serious arterial and venous thrombosis associated with pentosan polysulfate-induced thrombocytopenia: --two cases of fatal circumferential myocardial infarction due to disseminated thrombosis in patients whose coronary vessels were free from atheroma at angiography. Such cases have not previously been published. They seem to represent an unusual and dangerous manifestation of immunoallergic thrombocytopenia complicated by diffuse intravascular coagulation and induced by pentosan polysulfate; --two cases of myocardial infarction with favourable outcome; one of them was associated with hemiplegia with aphasia; --one case of extensive phlebitis of the inferior vena cava. The diagnosis was suspected on the ground that the patients had previously been treated with intramuscular pentosan polysulfate for 8 to 10 days and had less than 100,000 platelets per mm3; it was confirmed by in vitro platelet aggregation tests. Cross-allergy with heparin was present in all cases. Out of 18 published cases of pentosan polysulfate-induced thrombocytopenia, 15 were revealed by thrombosis of a coronary, cerebral or peripheral artery (80 p. 100) or of a vein (20 p. 100). Arterial thrombosis carries a 50 p. 100 risk of death, and for this reason pentosan polysulfate should be subjected to the same rules of prescription and monitoring as heparin.
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PMID:[Disseminated coronary thrombosis and thrombopenia induced by pentosan polysulfate]. 246 Nov 80

A case of moyamoya disease associated with thrombotic thrombocytopenic purpura (TTP) was reported. A 26-year-old male patient was admitted on April 11, 1992, with sudden onset of right cerebral hemorrhage. Cerebral angiography revealed moyamoya disease and bilateral encephalo-duro-arterio-synangiosis (EDAS) was performed. In March, 1993, however, he suffered from left cerebral hemorrhage. Neurological examination on the second admission showed disturbance of consciousness, motor aphasia and right hemiplegia. Emergency operation for the hematoma removal was performed and neurological functions rapidly improved. However, on the day following the operation, he was in stupor and restlessness. Microangiopathic hemolytic anemia and severe thrombocytopenia were identified and he gradually sank into a comatose state. Systemic purpura, fever, renal dysfunction also appeared. CT scan 22 days after the onset demonstrated diffuse cerebral infarction in the region of the bilateral anterior and middle cerebral arteries, and cerebral angiography on the next day demonstrated the development of bilateral internal carotid stenosis. Though laboratory findings indicate gradual improvement, he has remained in very weak state. This is the first case of moyamoya disease associated with TTP. The etiology of both diseases was discussed.
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PMID:[Moyamoya disease associated with thrombotic thrombocytopenic purpura (TTP)]. 801 79

Reye syndrome (RS) is an acute encephalopathy in childhood, and is very rare in adulthood. Here we report a 21-year-old woman with RS. Because of her dysmenorrhea, she took 3 tablets of diclofenac sodium (25 mg) per day in 3 divided doses for two days. Two days after the last intake of the medicine, she developed high fever, nausea, vomiting, and disturbance of consciousness with delirium, i.e., acute encephalopathy. She did not have seizure, hemiplegia, or other focal neurological manifestations. The serum GOT level was normal at onset, but in 12 hours dramatically increased up to 8,632 IU/L. The serum bilirubin level was normal. The cerebrospinal fluid revealed normal cell count, and protein. Although the liver biopsy was not performed because of thrombocytopenia, we diagnosed her as an adult case of RS according to the clinical criteria of the Center for Disease Control. In addition to treatment for the brain edema, plasma exchange was performed once treat the encephalopathy at the onset. The next day, her consciousness level and serum GOT level markedly improved. She completely recovered from acute encephalopathy in a week after her admission. In conclusion, diclofenac sodium, as well as aspirin, should be considered as a possible causal agent for RS, and early plasma exchange may be beneficial.
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PMID:[An adult case of Reye syndrome induced by diclofenac sodium, and recovered by plasma exchange]. 974 77

A young male patient who presented with steroid-responsive parkinsonism, hemiplegia, thrombocytopaenia and systemic illness who was subsequently diagnosed to have systemic lupus erythematosus (SLE) is described. He later developed post-hemiplegic dystonia. Thalamic lesions on magnetic resonance imaging (MRI) are demonstrated. Clinical features and neuropathology of central nervous system lupus are discussed. This is the first report of SLE presenting with Parkinsonism, and the first to demonstrate anatomically-relevant MRI lesions in Parkinsonism associated with SLE.Copyright Lippincott-Raven Publishers
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PMID:Systemic lupus erythematosus presenting with steroid-responsive parkinsonism and post-hemiplegic dystonia. 1021 Aug 49

A 30-year-old woman at 25 weeks gestation presented to the labour ward complaining of abdominal pain and a painful bruise in her right groin. Over the course of several hours, she developed rapidly spreading necrotising fasciitis of the right thigh. She required emergency radical debridement of the thigh and caesarean delivery of a dead fetus. She was admitted to the intensive care unit (ICU) with septic shock, where she received ventilatory and inotropic support. Streptococcus pyogenes was isolated from the infected tissue and a diagnosis of group A streptococcal toxic shock-like syndrome (GAS TS-LS) was confirmed. Following acute and rapid haemodynamic deterioration, plasmapheresis was given for 6 days, after which the patient's general condition improved and vasoconstrictor requirement was significantly reduced. Subsequently, immunoglobulin was given intravenously for thrombocytopenia, following which the platelet count steadily improved. Despite the development of acute renal failure, acute respiratory distress syndrome and a left hemiplegia, the patient made a remarkable recovery. She was later transferred to a plastic surgical unit for split skin-grafting. The importance of early diagnosis and aggressive treatment of GAS TS-LS is emphasized and the place of plasmapheresis and intravenous immunoglobulin therapy in this condition is discussed.
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PMID:Necrotising fasciitis and group A streptococcus toxic shock-like syndrome in pregnancy: treatment with plasmapheresis and immunoglobulin. 1532 Nov 56

A 53-year-old male was admitted because of pancytopenia and chronic subdural hematoma. Bone marrow was hypercellular with 97% blasts, which expressed CD10, CD19, CD20, and immunoglobulin mu and gamma chains on the cell surface and had chromosomal abnormalities including t(8 ; 22)(q24 ; q11). The patient was diagnosed as having Burkitt leukemia. Because hemiplegia and disturbance of consciousness developed rapidly, the patient was treated with an emergency drainage operation followed by Hyper-CVAD therapy and achieved a sustained complete remission. Dural infiltration of leukemic cells as well as thrombocytopenia was implicated in the pathogenesis of the subdural hematoma, which contained numerous blasts.
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PMID:[Successful treatment with drainage of hematoma and chemotherapy in a case of Burkitt leukemia presenting with subdural hematoma]. 1644 61

Cardiac and vascular intervention in thrombocytopenic congenitally cyanotic patients is more dangerous. Thrombocytopenia in these patients is related to immune thrombocytopenia, polycythemia, hyperviscosity, pseudothrombocytopenia, and drugs. Herein we report on a thrombocytopenic 8-year-old girl with tricuspid valve atresia and pulmonary valve stenosis admitted for catheterization. Thrombocytopenia (21,000/mm3) and shunt occlusion was noticed. Thrombocytopenia did not recover after intravenous immunoglobulin (IVIG) and phlebotomy therapies. During preparation for surgery, she suffered cardiopulmonary arrest. A Gore-tex graft was placed in the right pulmonary artery and truncus brachiocephalicus. After surgery, her platelet count spontaneously increased to within the normal range (178,000/mm3 to 250,000/mm3). After resuscitation, she had right-sided hemiplegia sequelae, though there were no hemorrhagic findings on cranial magnetic resonance imaging (MRI) or computed tomography (CT) scans. Two months after surgery, the Blalock-Taussig (BT) shunt blood flow decreased, thrombocyte count dropped, and peripheral cyanosis reappeared. A Fontan operation was performed without hemorrhagic events, and after surgery the thrombocyte count reached 330,000/mm3. We suggest that if a patient with cyanotic heart disease has thrombocytopenia and there is no apparent cause, hypoxia-related thrombocytopenia must be considered. After reoxygenation by shunt or corrective surgeries, thrombocyte count and functions will recover.
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PMID:Shunt operations improved thrombocytopenia in a patient with congenital cyanotic heart disease. 1898 52


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