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)

An infant with severe homozygous protein C deficiency was brought to medical attention because of purpura fulminans and severe bilateral vitreous hemorrhages in the neonatal period. Infusions of fresh frozen plasma were given for 8 months. On two occasions, attempts to decrease the frequency of fresh frozen plasma infusions to less than twice a day led to episodes of microangiopathic hemolysis, fibrinolysis, and acute renal failure. Infarction of skin and subcutaneous tissues did not recur. Both episodes were controlled after reinstitution of fresh frozen plasma. Complications of therapy with fresh frozen plasma included hyperproteinemia and hypertension. Warfarin therapy was instituted when the baby was 8 months of age, followed by a gradual withdrawal of fresh frozen plasma therapy. The dose of warfarin required to maintain the prothrombin time in a range of 1.8 to 2.2 times normal varied considerably during short periods, a phenomenon that may have been due to several factors: hypercatabolism of the drug with prolonged administration, abnormality of liver function, variation in levels of serum albumin, fluctuations in drug dosage secondary to oral administration, and variations in dietary vitamin K. Protein C determinations by immunologic and functional assays consistently showed detectable but reduced protein C antigen levels with undetectable activity levels, suggesting that a dysproteinemia rather than a deficiency of synthesis is responsible for the child's coagulopathy.
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PMID:Homozygous protein C deficiency: observations on the nature of the molecular abnormality and the effectiveness of warfarin therapy. 334 Apr 76

Two cases of complete sagittal sinus occlusion with multiple brain hemorrhages, elevated intracranial pressure, and disseminated intravascular coagulation are described. These patients were successfully managed using pentobarbital-induced coma to ameliorate intracranial pressure elevation. This therapy was combined with monitoring of intracranial pressure and intermittent drainage of cerebrospinal fluid to further control intracranial pressure elevations. Thrombus and coagulopathy resolved with pentobarbital alone in one patient and after pentobarbital plus heparin therapy in the second patient. It is suggested that cases of severe distal sagittal sinus thrombosis with brain hemorrhage and intracranial hypertension may benefit from combined pentobarbital coma and intraventricular drainage. This allows for stabilization of bleeding tendencies before instituting heparin therapy when necessary. Management of sagittal sinus thrombosis with barbiturates or ventricular drainage is best performed in an intensive care unit environment with continuous monitoring of intracranial pressure and substantial electrophysiologic and neuroradiologic support.
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PMID:Treatment of sagittal sinus thrombosis associated with cerebral hemorrhage and intracranial hypertension. 338 62

The incidence of deep-vein thrombosis was studied in 146 consecutive Korean patients who had a cementless total hip replacement with a porous-coated anatomic prosthesis. All of the patients had discontinued taking aspirin, aspirin-containing compounds, or other antiplatelet medications fourteen days before admission to the hospital for the operation. Deep-vein thrombosis was diagnosed by roentgenographic venography, and pulmonary embolism, by perfusion lung-scanning. There was an unusually low incidence (10 per cent) of deep-vein thrombosis in this series. In contrast to other reports, we did not identify a relationship between deep-vein thrombosis and so-called risk factors such as advanced age, number of venous valves (more than five) in the lower extremity, abnormal coagulation-assay data, certain diseases, or preoperative limitation of mobility. In addition, hypertension, blood group, surgical approach, and choice of cemented or cementless total hip replacement did not seem to affect the incidence of deep-vein thrombosis. There was a low incidence of deep-vein thrombosis in patients in whom obesity, prolonged immobilization postoperatively, varicose veins, and hyperlipemia were not factors.
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PMID:Low incidence of deep-vein thrombosis after cementless total hip replacement. 339 86

Two cases of adult respiratory distress syndrome were treated in a series of 26 patients suffering from colchicine overdose. The syndrome appeared between the 24th and 72nd hours. It was characterized by the presence of interstitial as well as alveolar oedema seen on chest roentgenograms. Haemodynamic investigation showed a hyperkinetic state with moderate precapillary pulmonary arterial hypertension. In addition, multivisceral phenomena were observed in all cases. Post-mortem examination revealed interstitial and alveolar pulmonary oedema with haemorrhagic or macrophagic alveolitis often accompanied by hyaline membrane. The physiopathology of ARDS occurring in colchicine poisoning appeared to involve such different factors as infection, the presence of a state of shock and disseminated intravascular coagulopathy. The direct toxic action of colchicine on pneumocyte microtubules and the inhibition of surfactant production were a probable cause. The responsibility of colchicine in leukocyte aggregation remains to be determined.
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PMID:[Acute respiratory distress syndrome in adults in colchicine poisoning]. 354 81

During approximately a 9-year period, 37 severe preeclamptic-eclamptic patients had pulmonary edema for an incidence of 2.9%. The incidence was significantly higher in older patients (p less than 0.0001) and in multigravid patients (p less than 0.05). Eleven (30%) had antepartum edema with 10 (90%) of the 11 having preexisting chronic hypertension. Twenty-six (70%) had postpartum edema with an average onset of 71 hours post partum. The majority of these patients had excessive colloid and crystalloid infusions for various medical, surgical, and obstetric complications. There were four maternal deaths and morbidity was significant. Eighteen patients had disseminated intravascular coagulopathy, 17 had sepsis, 12 had abruptio placentae, 10 had acute renal failure, six had hypertensive crisis, five had cardiopulmonary arrest, two had rupture of the liver, and two had ischemic cerebral damage. The overall perinatal mortality was 530/1000 and neonatal morbidity was significant. Pulmonary edema is infrequent in severe preeclampsia-eclampsia without associated medical, surgical and obstetric complications. The occurrence of pulmonary edema in such patients is associated with high maternal and perinatal mortality and morbidity.
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PMID:Pulmonary edema in severe preeclampsia-eclampsia: analysis of thirty-seven consecutive cases. 357 33

We reviewed the clinical and laboratory characteristics of 34 patients who had classical heatstroke during the Kansas City heat wave of 1980. The patients were elderly, predominantly black, and of low socioeconomic class. Overall mortality was 18%, with 9% of patients exhibiting severe residual neurologic deficit; 73% had full recovery. Patients with coma, temperature greater than or equal to 108 F (42.2 C), severe hypotension, coagulopathy, and need for respiratory assistance were at highest risk of death. Associated disease was common (67%), with hypertension (32%), diabetes (21%), and alcoholism (21%) being most frequent. Medications known to predispose to heatstroke were used by 56% of patients. Hematologic abnormalities were nonspecific, and clinical evidence of renal or hepatic failure was rare. Hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia, and elevated levels of creatine phosphokinase and glucose were frequent but did not correlate with outcome. The predominant arterial blood gas abnormality was metabolic acidosis or a combined metabolic acidosis and respiratory alkalosis.
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PMID:Classical heatstroke: clinical and laboratory assessment. 396 67

Plasma beta-thromboglobulin (BTG) was measured in 25 patients with pregnancy-induced hypertension (PIH), 7 of whom had severe PIH, and in 23 healthy gravidae. Also platelet counts, spontaneous platelet aggregation in vitro, and coagulation studies such as fibrinogen, fibrinogen degradation products and antithrombin III (AT III) were carried out: fetal outcome was judged by birthweight, placental weight and venous umbilical pH. Plasma BTG values of the PIH and severe PIH patients were significantly higher than those of the controls (P less than 0.05), suggesting enhanced platelet activation in the former. Compared with the controls, the entire PIH group was found to have significantly lower AT III values (P less than 0.05), more positive protamine sulphate tests (P less than 0.025), and higher plasma urate concentrations (P less than 0.01), but increased BTG values were more often observed than abnormal coagulation tests. No relationship could be demonstrated between the BTG level and fetal outcome. The significant increase in plasma BTG in PIH indicates enhanced platelet activation in these patients.
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PMID:Plasma beta-thromboglobulin in normal pregnancy and pregnancy-induced hypertension. 618 11

By activating plasminogen into plasmin, which in turn dissolves fibrin, fibrinolytic agents can dissolve pathologic thrombi. Streptokinase, a fibrinolytic agent derived from group C beta-hemolytic streptococci, is antigenic and can elicit allergic reactions. Urikinase, a fibrinolytic agent obtained by purification from human urine or from human fetal kidney cell culture, is not antigenic, and for this reason can be used repeatedly, if needed, whereas streptokinase cannot be used for retreatment within six months of a course of therapy. Either agent can be introduced into the circulation systemically (intravenously) or locally (via catheter). The indications for systemic therapy include deep-vein thrombosis, pulmonary embolism, and arterial thrombosis and embolism. The indications for local therapy include acute myocardial infarction, arterial thrombosis and embolism, and the clearing of occluded arteriovenous cannulae and access shunts. Contraindications include an actively bleeding lesion, a vascular intracranial disorder, or uncontrolled hypertension; relative contraindications include pregnancy; a recent wound, fracture, surgery, or deep closed biopsy; or a general contraindication to anticoagulation, such as coagulopathy, uremia, or severe liver disease. During thrombolytic therapy, invasive procedures, intramuscular injections, and the use of other anticoagulant or antiplatelet agents should be avoided. Measurement of fibrinogen levels, the titer of fibrin/fibrinogen degradation product, or thrombin time can be used to monitor therapy.
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PMID:Fibrinolysis and its current usage. 634 82

Hypertension may occur during pregnancy under different clinical circumstances. One cause is toxemia, a systemic disease unique to pregnant women, in which hypertension is associated with proteinuria, CNS irritability, hepatic and renal functional abnormalities, and, in fulminant disease, a consumptive coagulopathy. Since it is clear in the non-pregnant population that the vascular complications of hypertension can be prevented with antihypertensive therapy and since toxemia is the most common cause of maternal mortality, there is no reason not to treat pregnant women with hypertension.
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PMID:How should hypertension during pregnancy be managed? An internist's approach. 636 37

The purpose of the present clinical investigation was to determine the influence of aggressive management, associated medical/obstetric complications, race, and gestational age on fetal, neonatal, and maternal risks associated with severe preeclampsia. Three hundred and three consecutive pregnancies complicated by severe preeclampsia were studied. All patients were delivered within 48 hours after admission to the perinatal center. In 91 patients the disease was superimposed on chronic hypertension. There was a significant difference between patients with and those without prior chronic hypertension regarding perinatal mortality (32 versus 7.7%), incidence of abruptio placentae (10 versus 4%), and frequency of small-for-gestational-age infants (33 versus 14%). Fifty-one patients (17%) had thrombocytopenia, 26 (8.5%) had hemolysis, elevated liver enzymes and low platelet count syndrome, and 22 (7.3%) had disseminated intravascular coagulopathy. There was significant difference between white and black patients regarding the frequency of thrombocytopenia (28 versus 13%), hemolysis, elevated liver enzymes, and low platelet count syndrome (19.7 versus 5.3%), and coagulopathy (13 versus 1.4%). However, most of this apparent racial difference resulted from higher incidence of abnormal hematologic findings among patients who had conservative management by private physicians before transfer. Perinatal survival was zero when severe preeclampsia developed at or before 28 weeks, whereas it was 100% when disease developed after 36 weeks' gestation. The above factors should be considered in counselling patients with severe preeclampsia.
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PMID:Pregnancy outcome in 303 cases with severe preeclampsia. 646 61


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