Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anatomical location and appearance of retinal hemorrhages in the infant provide important clues in the diagnosis of underlying disorders. While neonatal retinal hemorrhages related to birth trauma are common, benign, and self-limited, other retinal hemorrhages in infancy may signify intracranial aneurysms, accidental or non-accidental injury, and a variety of ocular (e.g., Coats' disease, PHPV, ROP, retinal dysplasia, hypertension, myopia) or systemic disease (e.g., hematologic or cardiovascular disorders, infection, protein C deficiency). In this review, retinal hemorrhages are illustrated and classified according to location, appearance, and etiology. Prompt diagnosis of retinal hemorrhages in infants is crucial, because treatment may be required to prevent early deprivation amblyopia and blindness. Ophthalmological findings may also be a valuable contribution to the overall medical evaluation of the infant.
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PMID:Fundus hemorrhages in infancy. 150 54

In a study of biological risk factors for sudden death in patients with coronary artery disease, 320 patients were, prospectively, recruited and followed-up over two years. None of the patients had heart failure or recent myocardial infarction. The following variables were recorded: previous acute myocardial infarction, hypertension, smoking habits, ventricular arrhythmia; the angiographic variables included: left ventricular ejection fraction, Jenkins' and mean atherosclerotic scores; lipid profile: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoproteins Al and B; hemostatic profile: fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2-antiplasmin, euglobulin clot lysis time and tissue plasminogen activator before and after venous occlusion, tissue plasminogen activator inhibitor, platelet factor 4, beta-thromboglobulin. During the follow-up period, 12 of the patients died suddenly. In these patients, ejection fraction was lower: 49 +/- 16% versus 61 +/- 14% for the other patients (P less than 0.02), fibrinogen higher: 3.9 +/- 0.8 g/l versus 3.5 +/- 0.8 for the living patients (P less than 0.05) and protein C lower: 89 +/- 39% versus 111 +/- 39% (P = 0.06) for the other patients. In multivariate analysis: lower ejection fraction (P less than 0.008), older age (P less than 0.03) and lower protein C (P less than 0.01) were correlated with sudden death. Among the patients with coronary artery disease, the raised fibrinogen and the decreased protein C appeared to be risk factors for sudden cardiac death. These alterations reflected a prothrombotic state which might increase the ischemic risk, due to an acute thrombosis, leading to the fatal ventricular arrhythmia. Determination of these hemostatic variables might be a useful adjunct for assessment of the vital prognosis of patients with coronary artery disease, especially the risk of sudden death in addition to other known clinical, electrocardiographic, hemodynamic risk factors. This would also guide both the instigation of complementary investigations and appropriate therapy in such high risk group of patients.
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PMID:Biological risk factors for sudden death in patients with coronary artery disease and without heart failure. 156 56

Protein C together with its plasmatic cofactor protein S and antithrombin III probably represent the most important plasmatic inhibitor in coagulation. Protein C deficiency constitutes a high risk factor for venous thrombosis. Cerebral venous thrombosis is a manifestation which is scarcely referred to in protein C deficiency. The case of a 32 year old patient with protein C deficiency is presented. The patient was admitted for an endocraneal hypertension syndrome. CT and MR demonstrated multiple hemorrhagic cerebral infarctions. Arteriography confirmed vertebral venous thrombosis. Only six cases sufficiently documenting cerebral venous thrombosis due to protein C deficiency were found in the literature. In most cases coadjuvant factors exist predisposing thromboembolic disease. The present clinical case demonstrates the importance of considering protein C deficiency in the diagnosis of cerebral venous thrombosis in young adults.
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PMID:[Cerebral venous thrombosis and hereditary protein C deficiency]. 159 2

Protein C is a vitamin K-dependent regulator of blood coagulation. Activated protein C is regulated in plasma in large part by two inhibitors, protein C inhibitor and alpha 1-antitrypsin. Complexes of activated protein C with both inhibitors in plasma samples from subjects with normal or pathologic pregnancy were measured. In normal pregnancy we observed a progressive and significant increase in activated protein C/alpha 1-antitrypsin complex levels, from 9 +/- 3 ng/ml in the first trimester to 16 +/- 3 ng/ml in the third trimester, as well as an increase in alpha 1-antitrypsin plasma levels. In severe preeclampsia, but not in chronic hypertension with superimposed severe preeclampsia, there was a greater increase in activated protein C/alpha 1-antitrypsin levels (25 +/- 10 ng/ml) (p less than 0.001) and a decrease in protein C and protein C inhibitor levels as compared with normal pregnant women at similar gestational ages. These data show an increase in the activation of the protein C pathway in both normal and pathologic pregnancy and provide evidence for an enhancement of thrombin generation in severe preeclampsia compared with chronic hypertension with superimposed severe preeclampsia.
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PMID:Complexes of activated protein C with alpha 1-antitrypsin in normal pregnancy and in severe preeclampsia. 185 2

The presence of disseminated intravascular coagulation (DIC) in the syndrome of haemolysis, elevated liver enzymes and low platelets (HELLP) is debated. We assessed the occurrence of decompensated and compensated DIC (using predefined criteria) in 15 consecutive nulliparous pregnant patients with gestational hypertension combined with the HELLP syndrome and in 12 consecutive nulliparous controls with pregnancy induced hypertension (PIH) but without the HELLP syndrome. A combination of routine coagulation assays revealed the absence of decompensated DIC in all studied patients. However, using more specific and sensitive coagulation assays, compensated DIC was observed in all HELLP patients and in three patients in the control group. The mean values of antithrombin III, thrombin-antithrombin III complexes and protein C in the HELLP and the control group were 66 vs 87% (P = 0.0004), 21 vs 8 ng/ml (P = 0.0008) and 57 vs 90% (P = 0.0018) respectively. We conclude that HELLP patients show evidence of compensated DIC which may have pathophysiological significance for the observed organ damage.
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PMID:Coagulation studies in the syndrome of haemolysis, elevated liver enzymes and low platelets. 199 31

Lipodermatosclerosis of the lower extremity, with or without ulceration, is a common manifestation of severe venous disease and the result of sustained venous hypertension. The latter is generally a sequela of deep vein thrombosis. Factors that enhance clot formation or impair fibrinolysis contribute to the pathogenesis of venous disease. It is already established that faulty fibrinolysis may play a pathogenic role in patients with venous disease. We examined the possibility that patients with venous disease have abnormally low plasma levels of proteins C and S, two proteins whose deficiencies have been reported to cause an increased frequency of thromboembolic disease. Using immunologic and functional assays for plasma proteins C and S, we found that 4 (21%) of 19 patients with lipodermatosclerosis and leg ulcers had abnormally low levels of protein C or protein S. One of 7 patients with lipodermatosclerosis without ulceration had a profoundly depressed level of protein C and a history of cerebral stroke at a young age. Plasma levels of protein C were normal in five patients with arterial insufficiency severe enough to cause leg ulceration. We conclude that abnormally low plasma levels of proteins C and S may be found in patients with lipodermatosclerosis and venous ulceration. As with the abnormally low fibrinolytic activity in these patients, our findings indicate a possible propensity for increased thrombotic disease.
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PMID:Protein C and protein S plasma levels in patients with lipodermatosclerosis and venous ulceration. 203 43

The range of disorders affecting the cerebral veins and sinuses is increasing and now includes blood disorders, abnormalities in the patterns of blood flow, and infiltrative or inflammatory conditions, all of which may promote thrombosis. We describe 10 patients with cerebral venous thrombosis: two had protein S deficiency, one had protein C deficiency, one was in early pregnancy, and there was a single case of each of the following: dural arteriovenous malformation, intracerebral arteriovenous malformation, bilateral glomus tumours, systemic lupus erythematosus, Wegener's granulomatosis, non-Hodgkin's lymphoma. The recognition of such diverse aetiology may be importance since clinical features are non-specific, and may consist only of raised intracranial pressure, allowing confusion with 'benign intracranial hypertension'. The existence of effective treatment both for the thrombosis and for many of the underlying disorders makes early diagnosis essential. The prognosis of treated patients may be favourable.
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PMID:Cerebral venous thrombosis: new causes for an old syndrome? 214 67

In this study, blood coagulation and fibrinolytic parameters were measured in maternal blood and fetal umbilical cord blood in 200 normal pregnant women and in 46 with severe toxemia of pregnancy (Toxemia), and the relationships between fetal growth and concentrations protein C (PC), antithrombin-III (AT-III) and alpha 2-plasmin inhibitor (alpha 2-PI) were studied. 1. Significant increases in fibrin degradation products (FDP) and in plasminogen (Plg), AT-III and PC were found in maternal blood of Toxemia. A significant increase in AT-III and a decrease in alpha 2-PI and PC were observed in cord blood from these patients. 2. The platelet count (Pl) tended to be low in patients with Toxemia complicated by fetal growth retardation (IUGR). 3. Pl and fibrinogen (Fib) tended to be high in Toxemia complicated by normal fetal growth. 4. PC increased from early pregnancy, and a further increase was observed in the puerperium. 5. The PC concentration correlated with the AT-III but not with the alpha 2-PI concentration in maternal blood. 6. PC in cord blood was lower than that in maternal blood, and was correlated with AT-III and alpha 2-PI. 7. In patients with Toxemia, PC was reduced in both maternal and cord blood, and this correlated with AT-III as well as alpha 2-PI in maternal blood. 8. PC was low in Toxemia complicated by hypertension and proteinuria. These results suggest the involvement of FDP, AT-III, PC and Plg in the pathogenesis of Toxemia, and that the Pl, Fib, FDP and alpha 2-PI concentrations are related to fetal growth. Therefore, the PC and AT-III concentrations appeared to be a useful index for the blood coagulation and fibrinolysis in pregnant women and appeared to be important factors in the degree of Toxemia and IUGR.
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PMID:[Blood coagulation and fibrinolytic studies in patients with toxemia of pregnancy]. 227 12

We investigated the plasma levels of thrombin-antithrombin III complexes in women with uncomplicated pregnancy, patients with preeclampsia, gestational hypertension, and nonpregnant control subjects. In addition, we measured the coagulation inhibitors antithrombin III, protein C, and protein S. In normal pregnancy we observed a progressive increase in plasma thrombin-antithrombin III levels, and a decrease in protein S levels. In preeclampsia we observed increased thrombin-antithrombin III levels, reduced antithrombin III and protein C levels, and no further reduction of protein S compared with normal pregnancy. These new methods provide solid evidence for a prethrombotic state in normal pregnancy, especially in preeclampsia.
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PMID:Enhanced thrombin generation in normal and hypertensive pregnancy. 252 25

This study prospectively evaluates hypercoagulable states in patients under 51 years of age undergoing lower extremity revascularization for ischemia and assesses early outcome after operation. Twenty patients whose ages range from 23 to 50 years (mean 40.8 years) were identified prospectively who underwent lower extremity revascularization and evaluation of hypercoagulability. Fifteen patients were male (75%), 10 were black (50%), six had hypertension (30%), and four were diabetic (20%). All but two were cigarette smokers (90%). Seven aortoiliac procedures and 13 infrainguinal procedures were performed. Six patients had one or more abnormalities of regulatory proteins (protein S deficiency, four; protein C deficiency, three; presence of lupus-like anticoagulant, three; plasminogen deficiency, two). Eight of 17 patients in whom platelet aggregation profiles were obtained showed increased reactivity (47%). Only 4 of 17 patients (24%) were normal when tested for all parameters. Arterial or graft thrombosis developed in four of the 20 patients within 30 days after operation. Hypercoagulability was found in all four patients whose revascularizations failed. A high incidence of hypercoagulable states was found in patients under 51 years of age with lower limb ischemia requiring revascularization. Hypercoagulability may have contributed to early postoperative thrombosis of the vascular procedure.
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PMID:Hypercoagulable states and lower limb ischemia in young adults. 252 8


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