Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An outbreak of a haemorrhagic diathesis in cattle fed home produced hay is described. A similar syndrome was reproduced experimentally in calves by feeding them the hay. The experimental disease was characterised by increased prothrombin and partial thromboplastin times while the leucocyte and erythrocyte counts remained normal until the terminal haemorrhage. The calves ate well and grew well until the rapid onset of progressive weakness, stiff gait, mucosal pallor, tachycardia, tachypnoea and haematomata ending in sudden death. The absence of blood coagulation was seen at necropsy while petechial, ecchymotic and free haemorrhages were found in most organs. Particularly striking were massive ecchymotic haemorrhages on the peritoneal surface of the rumen, a bloody, gelatinous mass enveloping each kidney and extensive bruising, haemorrhage and haematomata in the subcutis of the limbs. In a second feeding trial the effects of various preparations of vitamin K1 and vitamin K3 were investigated. Oral administration of large quantities of vitamin K1 reduced the elevated prothrombin time; vitamin K3 acted less consistently. Analysis of the hay for trichothecene mycotoxins was negative but floral analysis revealed that sweet vernal grass (Anthoxanthum odoratum) comprised about 80 per cent of the hay. Dicoumarol was detected in the hay and in the serum and ruminal contents of the experimental calves. The diagnosis, treatment, control and importance of this syndrome in the United Kingdom are discussed.
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PMID:Haemorrhagic syndrome of cattle associated with the feeding of sweet vernal (Anthoxanthum odoratum) hay containing dicoumarol. 619 8

A case of a young women with paroxysmal nocturnal hemoglobin (PNH) who developed thrombosis of the cerebral veins after beginning a regimen of oral contraceptives is presented. She was 24 years old and presented with a 3-week history of frontal headache, neck stiffness, paraesthesiae of both arms, and weakness of the left leg. She had begun use of Microgynon 2 months before presentation, but had discontinued use when symptoms began. Hematological studies showed a shortened partial thromboplastin time, high fibrinogen and factor VIII levels, and prlonged euglobulin clot lysis time. Though this patient had a history of coagulation difficulties, it was not until after taking the estrogen-containing contraceptive preparation that PNH developed. The mechanism of thrombosis may be related to the liberation of thromboplastic material from hemolysed erythrocytes and to interaction between complement-sensitive platelets and complement components in plasma. It is suggested that the estrogen augmented the previously existing thrombotic condition in this patient, and that administration of estrogen-containing preparations should not occur in women with thrombotic disorders.
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PMID:Cerebral vein thrombosis and the contraceptive pill in paroxysmal nocturnal haemoglobinuria. 744 35

Erythema multiforme major and disseminated intravascular coagulation developed in a dog 24 hours after exposure to a d-limonene-based insecticidal dip. Clinical signs included severe lethargy and weakness, ulceration of the oral mucosa, and erythematous serpiginous, annular, and arciform lesions on the head, trunk, and limbs. Clinicopathologic abnormalities included leukocytosis with neutrophilia, normocytic normochromic anemia, thrombocytopenia, prolongation of prothrombin and partial thromboplastin times, increased fibrin degradation products, hypoproteinemia, hyponatremia, hypochloremia, azotemia, high serum alanine aminotransferase and alkaline phosphatase activities, and high serum bilirubin concentration. Despite intensive supportive care, the dog developed severe intrathoracic and abdominal hemorrhage and died. Necropsy revealed severe diffuse epidermal necrosis and widespread hemorrhage within organs. Insecticidal dips containing d-limonene have the potential to induce various toxic effects, including, possibly, erythema multiforme major, and should be used cautiously.
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PMID:Erythema multiforme major and disseminated intravascular coagulation in a dog following application of a d-limonene-based insecticidal dip. 759 26

Sheep given powdered Ferula communis variety brevifolia at dosage of 2.5 g/kg of body weight/d for 15 days developed classical clinical signs of intoxication: anorexia, somnolence, apparent weakness, and hemorrhage. Marked reduction of vitamin K-dependent coagulation factors and prolongation of prothrombin time and activated partial thromboplastin time were consistent with presence of ferulenol, a toxic coumarinic factor in the plant. Changes induced in the coagulation system developed by the second day of plant administration and were normal within 4 days after dosing was stopped. There was no evidence of primary liver damage or platelet malfunction. Of 6 intoxicated sheep, 2 died with only minimal evidence of hemorrhage.
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PMID:Ferula communis variety brevifolia intoxication of sheep. 787 79

We report a case of spinal subdural haematoma with neurological deficit in a 36-yr-old woman following Caesarean section for severe preeclampsia and placental abruption. She had been taking chronic trifluoperazine treatment for depression. Her activated partial thromboplastin time (aPTT) was 49 sec (normal = 26-36) but all other tests of coagulation were normal. Epidural anaesthesia was attempted but, despite a negative test dose, injection of local anaesthetic resulted in a generalized seizure and general anaesthesia was induced. Seventy-two hours after delivery, she was found to have bilateral leg weakness, urinary incontinence, absent rectal sphincter tone and asymmetrical leg reflexes. The diagnosis of spinal haematoma was confirmed by magnetic resonance imaging. She underwent emergency laminectomy and made a full neurological recovery.
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PMID:Spinal subdural haematoma in a parturient after attempted epidural anaesthesia. 826 79

Both experimental and clinical data have shown that coagulation disorders are common in patients with cancer although clinical symptoms occur rarely. A prethrombotic state is probably involved in the mechanism of metastatic spread. Anticoagulant treatment, with either warfarin or heparin, has been shown to have a positive influence in small cell lung cancer. The purpose of this study was to evaluate the prethrombotic state as a possible marker of the outcome of lung cancer. Pretreatment prothrombin time (PT), partial thromboplastin time (PTT), antithrombin III (AT-III), platelet blood count (P), fibrinogen (F) and D-dimer (DD) were prospectively recorded in a series of 286 consecutive patients with a new primary lung cancer. Other recorded variables (32 in all) consisted of a set of anthropometric, clinical, physical, laboratory, radiological and pathological data. All patients were carefully followed up, and their subsequent clinical course recorded. Spearman rank correlation tests between coagulation factors were weakly significant, or more often non-significant. The best correlation index was that between PT and PTT (ra = -0.25). Univariate analyses of survival showed that a prolonged value of PT (P = 0.00167) and higher values of F (P = 0.00143) and DD (P = 0.0005) were associated with a poor prognosis. A few, weak relationships between well-known prognostic variables and coagulation abnormalities were also found. Because of the weakness of this correlation pattern, coagulation factors emerged in all the Cox's regression analyses as important predictors of survival, regardless of the number and type of cofactors used. A prethrombotic state (depicted by a prolongation of PT and increase of DD) is confirmed in this study as an aggravating condition in lung cancer. Studies attempting to reverse possible haemostatic abnormalities with the use of anticoagulants are justified by the present data.
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PMID:Haemostatic abnormalities in lung cancer: prognostic implications. 964 Feb 38

We report the results of a feasibility study using intravenous magnesium sulphate for deliberate hypotension in 16 ASA 1 patients undergoing major oral and maxillofacial surgery. All the patients received a standard nitrous oxide, oxygen, isoflurane, opioid and muscle relaxant anaesthetic. Magnesium sulphate was infused at 40 g/h until the mean arterial pressure reached 55 +/- 5 mmHg, followed by a maintenance dose of 5 g/h until 30 minutes prior to the end of surgery. The mean arterial pressure was significantly (P < 0.01) reduced by the magnesium sulphate when compared to baseline values. Control of the mean arterial pressure was satisfactory. No patient had reflex tachycardia, cardiac arrhythmia or rebound hypertension. In 14 patients the surgeons thought that the blood loss was less than when using other hypotensive anaesthetic techniques. In 2 patients the surgeons thought the blood loss was excessive. In another 2 patients, the surgeons thought that there was excessive facial swelling on completion of surgery. Postoperative muscle weakness and sedation were not problems clinically. Fourteen patients were extubated immediately after surgery and another 2 patients an hour later in the recovery room. Intraoperative urine output was well maintained. On completion of surgery, the prothrombin time was significantly increased (P < 0.05), and the partial thromboplastin time significantly decreased (P < 0.05) in all the patients (when compared to preoperative values); the clinical significance of this is unclear. The use of intravenous magnesium sulphate for deliberate hypotension is feasible in ASA 1 patients using a standard nitrous oxide, oxygen, isoflurane, opioid and muscle relaxant technique. This study forms the basis for a larger controlled study where the issues of postoperative sedation and weakness and coagulopathy can be dealt with in greater detail.
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PMID:Is it feasible to use magnesium sulphate as a hypotensive agent in oral and maxillofacial surgery? 1010 49

A 70-year-old patient with a history of hypertension and hypercholesterolemia was referred for evaluation of necrotic toes. The patient had a history of several cerebrovascular accidents during the previous month. Initially, she developed sudden-onset left upper extremity weakness which, over the ensuing 4 days, progressed to complete left-sided weakness. This was followed by the development of acute dysarthria. A transesophageal echocardiogram revealed moderate left ventricular hypertrophy, several vegetations on her tri-leaflet aortic valve associated with moderate aortic regurgitation, and a large right atrial thrombus with a mobile component. Bubble studies failed to reveal any septal defects. The patient's electrocardiogram was nonspecific. As serial blood cultures were negative despite fevers of up to 39.8 degrees C, the patient was treated with a 6-week course of intravenous ceftriaxone, ampicillin, gentamicin, and ciprofloxacin for a presumed diagnosis of culture-negative endocarditis. Fungal cultures of the blood were negative. The patient, however, progressed and developed several necrotic toes. Physical examination was significant for ischemic changes of the left first, second, third, and fifth toes, as well as the right first and second toes. Diffuse subungual splinter hemorrhages in the toenails, numerous 2-4-mm palpable purpuric papules on the lower extremities, and nontender hemorrhagic lesions of the soles were also noted. Peripheral and carotid pulses were intact and no carotid bruits were heard. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic examination revealed a disoriented, dysarthric patient with left central facial nerve paralysis, as well as spasticity, hyperactive reflexes, and diminished strength and sensation in the left upper and lower extremities. A left visual field defect and left hemineglect were also present. The patient's last brain computerized tomogram revealed areas of low attenuation consistent with cerebral infarctions in three distinct areas of the brain. These included the left occipitotemporal area, the right parieto-occipital area, and the right posterior frontal region. The regions affected were in the distribution of both the anterior and posterior circulation. No evidence of hemorrhage was noted. The patient subsequently complained of abdominal discomfort. A computerized tomogram of the abdomen with oral and intravenous contrast revealed a 4-cm x 3-cm irregular mass in the tail of the pancreas with several low-attenuation lesions throughout the liver which were consistent with infarctions or metastases. Several splenic infarctions were also present. A biopsy of the tumor revealed pancreatic adenocarcinoma. The patient's carcinoembryonic antigen level was 18. 4 ng/mL (0-3) and the CA 19-9 antigen level was 207,000 U/mL (0-36). The alpha-fetoprotein level was normal. Other significant laboratory findings included a prothrombin time of 16.7 (international normalized ratio, 1.4), an activated partial thromboplastin time of 32 (ratio, 1.3), and a platelet count of 85,000/mm3. The Russell viper venom time, sedimentation rate, and C3 levels were normal, and the patient was negative for antinuclear antibodies, anticardiolipin antibodies, and antibodies to extractable nuclear antigens. Of note, the patient was not receiving any anticoagulation. Blood cultures for mycobacteria and fungi, human immunodeficiency virus serology, and urinalysis and culture were negative. The patient subsequently developed an inferior wall myocardial infarction and was transferred to the coronary care unit. In line with the family's request, aggressive care was ceased and the patient expired. The patient's family refused an autopsy.
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PMID:Cutaneous manifestations of marantic endocarditis. 1080 80

A review of 60 cases of immune-mediated hemolytic anemia (IMHA) in the dog was performed in order to characterize the disease and to identify potential prognostic indicators. Dogs ranged in age from 1 to 13 years, with a mean age of 6.5 years. The 2 most commonly affected breeds were Cocker Spaniels and Labrador Retrievers. Fifty-two of the 60 dogs tested (87%) were autoagglutination positive and spherocytes were present in 45 (75%). Forty-one (89%) of 46 patients tested positive for the presence of immunoglobulin on the red blood cell surface (Coombs assay). The most common clinical signs at presentation were lethargy, weakness, pale mucous membranes, icterus, hemoglobinuria, and anorexia. PCV less than 25% was present in 59 (98%) dogs. At the time of presentation, 35 dogs (58%) had a nonregenerative anemia, whereas 25 patients (42%) had a regenerative response. Thrombocytopenia was seen in 41 (68%) dogs. Nine of 34 dogs (26%) had a prolonged prothrombin time, 19 of 34 (56%) had a prolonged activated partial thromboplastin clotting time, and 12 of 34 (35%) had abnormal fibrinogen concentrations. All dogs received prednisone at immunosuppressive doses (2.2-4.4 mg/kg PO as a single or divided dose every 24 hours) and cyclophosphamide as primary therapy. Forty-one dogs (63%) received cyclophosphamide at 50 mg/m2 q24h for 4 days, whereas 9 dogs (15%) received an initial high dose (200 mg/m2) followed by 3 days of a lower dose (50 mg/m2 q24h). No statistical difference in survival times was found for either protocol. Thirteen dogs were treated with azathioprine in addition to cyclophosphamide and prednisone. The median survival time of dogs that received all 3 drugs was 370 days as compared to 9 days for those dogs that were treated with cyclophosphamide and prednisone alone. Thirty-one (52%) dogs died from the disease, 13 (22%) dogs were alive, and 15 (25%) dogs were lost to follow-up. The median length of survival for all dogs was 21 days. Eight dogs that were discharged from the hospital suffered a relapse (PCV < 25%).
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PMID:Treatment of immune-mediated hemolytic anemia in dogs with cyclophosphamide. 1093 98

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62


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