Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Levels of the plasmin-alpha 2-plasmin inhibitor complex (PLN-A2PI complex) and alpha 2-plasmin inhibitor (A2PI) were determined by enzyme-linked immunosorbent assay (ELISA) with monoclonal antibodies in 59 patients with 66 chronic subdural hematomas (SDH's). Normal concentrations of the PLN-A2PI complex and A2PI in plasma are below 0.8 microgram/ml and 60.5 +/- 16.1 micrograms/ml, respectively (mean +/- 2 standard deviations). The hematoma fluid contained high concentrations of the PLN-A2PI complex (4.58 +/- 2.60 micrograms/ml) and low concentrations of A2PI (10.32 +/- 4.81 micrograms/ml), while both values in the plasma of 12 patients with chronic SDH's were within the normal range. This represents local hyperfibrinolytic activity in the hematoma. Stuporous or comatose patients had higher PLN-A2PI complex levels than did the alert and the drowsy or disoriented patients. The layering type of hematoma as seen on computerized tomography scans showed the highest PLN-A2PI complex levels among five types of hematoma. In the fluid drained postoperatively from the subdural cavities of chronic SDH's, both the PLN-A2PI complex and A2PI levels decreased gradually in healing cases. In two patients with hematoma reaccumulation after surgery, both levels increased. The postoperative increase of the PLN-A2PI complex represents the recurrence of intermittent cycles of fibrinolysis, bleeding, coagulation, and hemostasis in the subdural space.
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PMID:Plasmin-alpha 2-plasmin inhibitor complex and alpha 2-plasmin inhibitor in chronic subdural hematoma. 252 Dec 47

The case of a 26 year old woman who had been taking tranexamic acid to prevent uterine bleeding due to an IUD and who died from thrombosis of the left internal carotid artery is reported. The patient's father had died at age 54 of myocardial infarction. Otherwise the family history was entirely negative for thromboembolic disease. The patient was a mild smoker. She had been previously healthy and in particular, she was not affected with hypertension, diabetes, or dyslipidemia. She had carried to term 2 uncomplicated pregnancies. 40 days prior to hospital admission her gynecologist had inserted an IUD. The insertion of the IUD was followed by persistent uterine bleeding, and for this reason she began treatment with tranexamic acid (1.5 g/daily). Uterine bleeding persisted despite this treatment, and the IUD was removed. Because of persistence of a mild uterine bleeding, tranexamic acid was continued. 2 hours before admission the patient suddenly presented a left sided hemiparesis with disarthria and vomiting. On admission she was stuporous. The left side of her face drooped and the strength of the left arm and leg was markedly decreased. Both arm and leg reflexes were symmetrical. Her blood pressure was 110/70. An electroencephalogram on arrival confirmed a right sided cerebral lesion. Subsequently the patient's condition deteriorated rapidly. She developed a full left hemiplegia and became deeply comatose. A CAT scan performed 4 hours after admission showed no abnormalities. A CAT scan performed 3 days after admission showed a large cerebral infarction involving nearly the whole right cerebral hemisphere. The patient's condition remained essentially unchanged until she died 6 days after admission. Permission for autopsy was refused. Antifibrinolytic drugs competitively inhibit plasminogen activators and noncompetitively plasmin. Thromboembolic complications after the administration of antifibrinolytic drugs have long been recognized. The use of IUDs is often associated with troublesome uterine bleeding and particularly excessive menstrual bleeding. To avoid these complaints, antifibrinolytic drugs are increasingly used.
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PMID:Tranexamic acid, intrauterine contraceptive devices and fatal cerebral arterial thrombosis. Case report. 710 62