Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five patients (10 neonates, 15 children) with cerebral venous thromboses diagnosed by magnetic resonance imaging or computed tomography over a 10-year period were reviewed retrospectively. Two groups were analyzed separately because of their differing modes of presentation and outcome. Eighty percent of neonates presented with seizures and the outcomes were unfavorable in more than 50%. Thrombosis usually was associated with an acute systemic illness, such as shock or dehydration. In comparison, headache was the most common mode of presentation in the older children (excluding infants) and their outcomes generally were favorable. Thrombosis in this group usually occurred in the setting of a hypercoagulable state or an infectious process. In both groups, global or focal neurologic findings on initial examination unrelated to increased intracranial pressure correlated with the presence of an infarction on computed tomography or magnetic resonance imaging. Infants and children with infarction due to a deep venous thrombosis often had persistent neurologic disability at subsequent examination. No sequelae were observed in those children and neonates only with thrombosis or with superficial venous infarction. Treatment for both groups was conservative. No patient was anticoagulated specifically for the thrombosis. The good outcomes in most patients suggest that acute anticoagulation may not be indicated.
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PMID:Cerebral venous thrombosis in neonates and children. 158 Sep 53

Careful interpretation of the vascular pathology is important in cases of intestinal ischemia caused by primary mesenteric vein thrombosis because it suggests antithrombin III (AT III) deficiency. This deficiency, an autosomal dominant hereditary disorder, predisposes the patient to venous thrombosis. Similar or acquired deficiencies may also predispose the patient to thrombosis. In hereditary AT III deficiency, 90% of the cases have thrombosis of the leg or iliac veins; 8.3% of the cases, thrombosis of the mesenteric veins. Additionally, some families have a tendency to develop mesenteric vein thrombosis specifically. In this case report, a daughter with probable AT III deficiency had a history of 3 episodes of deep vein thrombosis in the previous 5 years while taking oral contraceptives. Her father, with the same deficiency, died from massive intestinal infarction resulting from portal and mesenteric vein thrombosis. The 19-year old woman developed gradually worsening abdominal pain, signs of peritonitis, and hematemesis. A laparotomy revealed peritonitis that was due to segmental small-bowel infarction; the underlying pathologic condition was mesenteric vein thrombosis. Coagulation study results revealed AT III activity by chromogenic assay, 0.48 u/mL; AT III antigen, 0.5 u/mL; and protein C antigen, 1.15 u/mL. 10 days after discharge, she developed a hemicranial headache with nausea, vomiting, neck tenderness, and photophobia; she was readmitted. A CT scan showed a left posterior parietal cerebral infarct. Repeat AT III activity by chromogenic assay was 0.51 u/mL and AT III antigen level was 0.50 u/mL. Before anticoagulant therapy could be initiated, the patient died 7 days after readmission. The combined lowering of AT III activity and antigen levels to half of normal suggests AT III deficiency. Earlier diagnosis of this deficiency could have been made in light of the patient's own history of thrombosis and the paternal history.
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PMID:Mesenteric venous thrombosis due to antithrombin III deficiency. 333 17

A case of cerebral venous thrombosis with familial antithrombin III (AT III) deficiency was reported and we discussed the anticoagulant therapy of cerebral venous thrombosis from the viewpoint of AT III. The patient, a 17-year-old boy, was admitted to our clinic with severe bifrontal headache, generalized convulsions and progressive disturbance of consciousness. He developed deep vein thrombosis in his right leg and pulmonary emboli two years earlier when he was placed on heparin and so forth, followed by warfarin sodium. Warfarin was terminated 9 months prior to his recent illness. On neurological examination on admission, he was semicomatous with blurred disc margins, roving eye movements with right abducens nerve palsy, nuchal stiffness and right flaccid hemiplegia. Left carotid angiogram and CT scan revealed extensive superior sagittal sinus thrombosis, complicated with hemorrhagic infarcts in bilateral frontal lobes. When examined for coagulation studies, the patient and his father had decrease in AT III activity and antigen levels. He was treated successfully with antiedematous agents and anticonvulsants during acute phase of illness. He was thereafter placed on warfarin 5-6 mg/day with no further clinical thromboembolic event for 2 years 9 months. There was no neurological abnormality when he was last examined, although he was treated with valproic acid 1,200 mg/day and phenytoin 250 mg/day to control occasional adversive seizures. A coagulation study following infusion of 5,000 units of AT III was carried out. Warfarin was discontinued the day before the study. 0.64 U/kg of AT III administration resulted in a 1% increase in AT III level after the infusion. The biological half life of AT III was 14.4 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral venous thrombosis with familial antithrombin III deficiency]. 404 Dec 90

Drug companies have been at work throughout the 1960s, 1970s, and 1980s trying to reduce the steroid content of their oral contraceptives (OCs). Researchers have been successful in reducing steroid content while maintaining effectiveness, thereby making OCs safer. In the 1st half of the natural menstrual cycle, a woman secretes estrogen as the dominant steroid product. In the 2nd half, estrogen is the principal reproductive hormone. Estrogens inhibit ovulation, possibly by inhibiting implantation, altering ovum transplant, or in some way preventing corpus luteum function, which is necessary to maintain early pregnancies and the endometrium. There are still only 2 estrogens and 6 progestins on the market today. They are probably the most thoroughly studied chemical ever seen in the history of pharmacy or medicine. 1 of the estrogens, mestranol, is really a drug of the past. In the body, mestranol is converted to ethinyl estradiol, the other estrogen on the market. Consequently, there is no reason to use mestranol itself. Within the dose range of 50-100 mcg, there's little difference in contraceptive effect. Progestins are the other active ingredient in the combination OC. Their principal action is the thickening of the cervical mucus, which prevents sperm penetration. Also, with sufficient progesterone, ovulation is inhibited, but this happens in only 40% of those patients taking, for instance, the "mini-pill" (which consists of progesterone only). The progestins and the estrogens work in concert to make OCs a highly effective contraceptive method. Recent surveys conducted by the Centers for Disease Control and National Cancer Institute looked into the relative effectiveness of OCs. Nordette had a use effectiveness failure rate of 3.5; Ovral, 3.6. Loestrin 1/20 -- norethindrone acetate, 1 mg, and estinyl estradiol, 20 mcg -- shows a failure rate of 4.5. This indicates that the threshold for an effective dose of estinyl estradiol in OCs is 30 mcg. For 1 mini-pill, Ovrette, the failure rate is 9.5 -- much higher. Depo-Provera has a failure rate of 0.7. The primary complaint from women taking OCs is spotting and breakthrough bleeding during the cycle. 30-50% of women given OCs stop taking them within a year. OC side effects include nausea, fluid retention, breast tenderness, leukorrhea, hypomenorrhea, headaches, spotting around the face, hypertension, and visual changes. 1 of the risks of birth control pills may be cervical dysplasia -- changes in the cells of the cervix. The relative risk of cervical cancer with OCs after 5-9 years is approximately 1.8. Clinical cases of deep vein thrombosis number 1/1000 per year among nonusers of OCs. Among users, the rate is 3 times as high: 3/1000. The most serious potential adverse effect is myocardial infarction. Of the excess deaths attributed to OCs (23.3 total per 100,000 users), 22.7 are due to myocardial infarctions and hemorrhage. The discussion also briefly reviews other methods of contraception -- Depo-Provera, male contraceptives, implants, the diapragm, and IUDs.
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PMID:Prescription contraceptives: countering the risks. 405 Jun 70

Twenty-five adults who harbored malignant gliomas received 72 courses of intraarterial 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) (100 mg/m2) and 67 courses of systemic vincristine (1.0 mg/m2) and procarbazine (100 mg/m2) as induction therapy (BVP) followed by 106 courses of systemic 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (methyl-CCNU) (130 mg/m2), vincristine, and procarbazine as maintenance therapy (MVP). With a 6-week interval between each treatment, the median and range for the number of courses of BVP were 3 and 1 to 4 and those for MVP were 3 and 0 to 14, respectively. Fifteen patients (60%) responded to both BVP and MVP, and 10 (40%) did not. The overall median survival time was 12.7 months (range, 1.8 to 48.5+ months). Two of 3 patients who had recurrent gliomas responded and survived for 37+ to 45+ months. Seven of 10 who had nonirradiated glioblastomas responded and survived for 9 to 22 months. Four who had nonirradiated anaplastic astrocytomas all responded and survived for 38+ to 48.5+ months. Two who also received radiotherapy (1 glioblastoma and 1 primitive neuroectodermal tumor) benefited and survived for 16.9 and 28.5+ months. All who did not respond favorably died within 8 months. During the infusion of BCNU, complications included transient orbital and head pain, periorbital and scleral erythema in all patients, and a focal seizure in 1 (4%). During the 6-month induction periods, leukopenia and thrombocytopenia occurred in 1 (4%), deep vein thrombosis occurred in 9 (36%), pulmonary emboli occurred in 8 (32%), upper respiratory infections occurred in 6 (24%), pneumonia occurred in 9 (36%), and herpes zoster occurred in 1 (4%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intraarterial 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and systemic chemotherapy for malignant gliomas: a follow-up study. 631 73

Orally administered dipyridamole in combination with naproxen was compared with subcutaneously administered low-dose heparin in prevention of deep venous thrombosis after abdominal hysterectomy. The radioactive fibrinogen test was used to diagnose thrombosis. Only one patient in the total series of 65 developed thrombosis. She belonged to the dipyridamole-naproxen group; the oral intake of the agents was disturbed by postoperative gastrointestinal side-effects. Vomiting and headache were more common in the dipyridamole-naproxen group, but wound complications (haematomas, ruptures and infections) were more common in the low-dose heparin group.
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PMID:Prevention of venous thrombosis by dipyridamole-naproxen and low-dose heparin in patients undergoing hysterectomy. 675 6

Lupus anticoagulant has been described in association with many autoimmune disorders. Here we describe its occurrence in a patient with ANCA-associated microscopic polyarteritis with medium vessel involvement. A 62-year-old man presented with mononeuritis multiplex and abdominal pain and was demonstrated to have multiple aneurysms on visceral angiography, consistent with the diagnosis of medium vessel vasculitis or classical polyarteritis nodosa. In addition he had active tuberculosis. He developed a deep venous thrombosis at this admission and, on one occasion, had a prolonged APTT but this was not confirmed to be due to a lupus anticoagulant. Two years later when the patient was readmitted with fevers, headaches and nasal discharge, both ANCA and a lupus anticoagulant were demonstrated in his serum, although there was no evidence of a venous thrombosis. Six months later the patient was demonstrated for the first time to have dysmorphic urinary RBC consistent with glomerular bleeding; at the same time he developed a deep venous thrombosis. ANCA was still present, but the lupus anticoagulant could not be detected. The patient was treated with cyclophosphamide and prednisolone and a Greenfield filter inserted into his inferior vena cava.
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PMID:Lupus anticoagulant in anti-neutrophil cytoplasmic antibody-associated polyarteritis. 773 54

A patient suffering from migraine, whose symptoms were abolished by warfarin therapy, is reported. Warfarin was prescribed for deep vein thrombosis and the frequency of the patient's headache improved remarkably during the anticoagulant therapy. Because of the unusual nature of the response to anticoagulant therapy, warfarin was reintroduced on a double blind (versus placebo) basis and once again abolished the headaches.
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PMID:Warfarin treatment and migraine. 814 17

A 34-year-old woman with a long-term history of amenorrhoea, headache and visual disturbances was operated for a hypothalamic tumor which could be completely removed. Postoperatively the patient developed a transient SIADH-syndrome and deep vein thrombosis; otherwise the clinical course was uneventful. There has been no sign of tumor recurrence at a follow-up period of fifteen months. Histological examination of the tumor revealed an ectopic pituitary adenoma with production of ACTH and TSH shown by immunohistochemistry.
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PMID:ACTH and TSH producing ectopic suprasellar pituitary adenoma of the hypothalamic region: case report. 839 55

Intravenous immune globulin (IVIg) is advocated as a safe treatment for immune-mediated neurologic disease. We reviewed the medical records of 88 patients who were given IVIg for a neurologic illness. Major complications in four patients (4.5%) included congestive heart failure in a patient with polymyositis, hypotension after a recent myocardial infarction, deep venous thrombosis in a bed-bound patient, and acute renal failure with diabetic nephropathy. Other adverse effects included vasomotor symptoms 26, headache 23, rash 5, leukopenia 4, fever 3, neutropenia 1, proteinuria (1.9 g/day) 1, viral syndrome 1, dyspnea 1, and pruritus 1. Fifty-two patients (59%) had some adverse effect of IVIg infusion, most commonly vasomotor symptoms, headaches, fever, or shortness of breath in 40 (45%), which improved with reduced infusion rate or symptomatic medications. Five (6%) had asymptomatic laboratory abnormalities and seven (8%) had other minor adverse effects. Adverse effects led to discontinuation of therapy in 16% and permanent termination of therapy in 10% of patients. There was no mortality or long-term morbidity. Although adverse effects were frequent, serious complications were rare except in patients with heart disease, renal insufficiency, and bed-bound state.
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PMID:Complications of intravenous immune globulin treatment in neurologic disease. 930 72


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