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

---

Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HELLP syndrome belongs to the group of pathological disorders associated with pregnancy-induced hypertension and may accompany preeclampsia. The basic criteria for establishing the diagnosis are as follows: H--for hemolysis, EL--for elevated liver enzymes and LP--for low platelets. In this report the authors present the case of a 32 years old primipara admitted to the Obstetrics Clinic complaining of epigastric pain, nausea and vomiting. Medical history revealed previously diagnosed and treated reflux disease. In the 39th week of gestation epigastric pain manifested again, blood pressure was high (150/100) and on the basis of laboratory parameters HELLP syndrome was diagnosed (GPT 319 U/L, GOT 204 U/L, platelet 80 x 10(9)/L, antithrombin III 63.9%, D-dimer (+++)). With this case report, authors wished to point out the importance of early diagnosis and treatment of this rare, but having high percentage of perinatal mortality syndrome.
...
PMID:[Pregnancy complicated by HELLP syndrome]. 1588 97

We treated a 59-year-old woman presenting with hemoptysis, a rare symptom of pheochromocytoma. Multiple factors including hypertension caused by sudden catecholamine release may result in pulmonary edema. It should be noted that the increased activation of coagulation cascade, which was demonstrated by increased thrombin-antithrombin III complex (TAT) and prothrombin fragment factor 1 and 2 (F1 + 2), as well as endothelial or platelet stimulation evidenced by the increased plasma von Willebrand factor, may have contributed to hemoptysis. These abnormalities were normalized after adrenalectomy. Our case indicates the important role of catecholamine in coagulopathy and possibly in vasculopathy.
...
PMID:A pheochromocytoma causing limited coagulopathy with hemoptysis. 1595 97

About 90% of cases of hemorrhagic uremic syndrome (HUS) occur in early childhood and most frequently are preceded by bloody diarrhea due to shiga-like toxin (SLT) producing Escherichia coli. We report a case of a newborn girl presenting with bloody diarrhea on her 7th day of life. Acute renal failure, severe arterial hypertension and hemolytic anemia were detected and prompt peritoneal dialysis and antihypertensive therapy were required. The girl had several episodes of seizures, necessitating intravenous phenobarbital. Transfontanel ultrasonography 48 h after disease onset was normal, whereas, MRI investigation 10 days later revealed severe ischemic lesions with beginning cystic encephalopathy. Renal function recovered and only very moderate tubular dysfunction remained. Serum analysis of factor H, von Willebrand factor protease, homocystinemia, proteins C and S, and antithrombin III were all normal. Mutation analysis of factor V Leiden, factor II, and methyltetrahydrofolate-reductase were normal. E. coli 0157:H7 and SLT 2 were detected in the stool. SLT 2 was also found in the mother's stool. This is the first report of mother-to-child transmission of SLT-producing E. coli.
...
PMID:Neonatal hemolytic uremic syndrome after mother-to-child transmission of Escherichia coli O157. 1601 May 98

As a risk factor for cardiovascular and cerebrovascular disease, hypertension and hyperlipidemia are believed to provoke vascular damage leading to a hypercoagulative state. The aim of the present study was to investigate the coagulative and fibrinolytic activity and hepatic mRNA expression of the coagulative factors in spontaneously hypertensive and hyperlipidemic female rats (SHHR:>150 mmHg of systolic blood pressure, >150 mg/dl of plasma cholesterol). Plasma levels of fibrinogen, thrombin-antithrombin III (ATIII) complexes and ATIII in the SHHR at 9 months of age increased significantly compared with those of age-matched Sprague-Dawley rats (SD). In the SHHR, the hepatic mRNA expression of the alpha- and beta-chains, but not the gamma-chain of fibrinogen and prothrombin was significantly enhanced. Therefore, the hyperfibrinogenemia in the SHHR was demonstrated to be due to the increase in hepatic mRNA expression of alpha- and beta-chains of fibrinogen. The pathological findings of the aortic arch from the 9-month old SHHR were cytoplasmic vacuolization and intimal thickening in the endothelium. These results suggest that hypercoagulation concomitant with the increase in hepatic mRNA expression of fibrinogen components may contribute to the development of atherosclerosis in the SHHR.
...
PMID:Enhancement of the coagulation system in spontaneously hypertensive and hyperlipidemic rats. 1614 22

Thromboembolic risk of atrial flutter (AFl) types has not been elucidated sufficiently in previous reports. The authors classified the patients according to surface electrocardiogram and electrophysiologic characteristics as those with typical AFl (37 patients, 78.4% male, mean age 59.8 +/-9.5 years) and atypical AFl (13 patients, 69.2% male, mean age 60.9 +/-6.9 years) and compared them regarding some clinical, echocardiographic, and hematologic parameters. An age- and gender-matched control group composed of 20 individuals without any organic heart disease in sinus rhythm was chosen (80% male, mean age 60.3 +/-7.9 years). Clinical features such as age, gender, organic heart disease, hypertension, diabetes mellitus, AFl duration, and the prevalence of paroxysmal atrial fibrillation were similar in both AFl groups. Echocardiographic parameters such as left ventricular ejection fraction, left atrial (LA) diameter, LA spontaneous echo contrast, and LA appendage emptying velocities were similar in both AFl groups. Fibrinogen, fibrin D-dimer, and thrombin-antithrombin III levels reflecting coagulation system activity were found to be increased in the patients with atypical AFl when compared with those with typical AFl and the control group (p < 0.001). In Pearson's correlation analysis, significant correlation between these hematologic markers and clinical and echocardiographic parameters were not found (p > 0.05). The coagulation system activity was found to be increased in patients with atypical AFl. Thus, anticoagulation due to the increased thromboembolic risk should be considered in patients with atypical AFl.
...
PMID:Do different atrial flutter types carry the same thromboembolic risk? 1619 99

The existence of an association between idiopathic intracranial hypertension (IIH) and coagulation disorders in men was assessed prospectively. Microthrombi, associated with thrombophilia-hypofibrinolysis, occlude arachnoid sinus villi, thus reducing resorption of cerebrospinal fluid, leading to IIH. Ten consecutively referred men with IIH, nine whites, one African American, median age 36 years, were 2 to 1 matched by age and race by healthy male controls. Polymerase chain reaction assays were done for four thrombophilic and one hypofibrinolytic gene mutations: G1691A factor V Leiden, G20210A prothrombin, C677T MTHFR, platelet glycoprotein IIb/IIIa (PL A1/A2), and 4G/5G polymorphism of the plasminogen activator inhibitor (PAI-1) gene promoter. Coagulation measures in plasma included dilute Russel's viper venom time (dRVVT), activated partial thromboplastin time (aPTT), the lupus anticoagulant, factor VIII, factor XI, plasminogen activator inhibitor activity (PAI-Fx), protein C antigenic, protein S total (antigenic), protein S free (antigenic), antithrombin III (functional), and resistance to activated protein C (RAPC). Tests performed on serum included anticardiolipin antibodies, homocysteine, and Lp(a). The body mass index was 40 kg/m(2) or greater (extremely obese) in two men, 30 to 40 kg/m(2) (obese) in three, and was 25 to 30 kg/m(2) in five (overweight). Cases differed from controls for inherited 4G4G homozygosity of the PAI-1 gene, four of 10 (40%) vs. one of 20 (5%), Fisher's p [p(f)]= .031, and for high levels (>21.1 U/mL) of the hypofibrinolytic PAI-1 gene product, PAI-Fx, 5 of 10 (50%) vs. one of 18 (6%), p(f) = .013. Thrombophilic factor VIII was high (> or = 150%) in three of 10 (30%) cases vs. zero of 16 (0%) controls, p(f)=. 046. The thrombophilic lupus anticoagulant was present in two of 10 (20%) cases vs. zero of 32 (0%) controls, p(f) = .052. Heritable hypofibrinolysis and heritable and acquired thrombophilia appear, speculatively, to be treatable etiologies of IIH in men. Understanding contributions of hypofibrinolysis and thrombophilia to the development of IIH should facilitate development of novel new approaches to treat this often-disabling neurologic disorder.
...
PMID:Idiopathic intracranial hypertension: associations with thrombophilia and hypofibrinolysis in men. 1624 70

The role of thrombophilia in the pathogenesis of preeclampsia is controversial. The aim of this case-controlled study was to determine whether thrombophilia increases the risk of preeclampsia or interferes with its clinical course. A total of 808 white patients who developed preeclampsia (cases) and 808 women with previous uneventful pregnancies (controls) matched for age and parity were evaluated for inherited and acquired thrombophilia (factor V Leiden; factor II G20210A; methylenetetrahydrofolate reductase C677T; protein S, protein C, and antithrombin III deficiency; anticardiolipin antibodies; lupus anticoagulant; and hyperhomocysteinemia). Odds ratios (ORs) with 95% confidence intervals (CIs) for risk of being carriers of thrombophilia in cases compared with controls and for risk of maternal life-threatening complications and adverse perinatal outcomes in preeclamptic patients with or without thrombophilia were calculated. Women with severe preeclampsia (406 cases) had a higher risk (OR, 4.9; 95% CI, 3.5 to 6.9) of being carriers of either an inherited or acquired thrombophilic factor, except for protein S, protein C, and antithrombin deficiency. In women with mild preeclampsia (402 cases), only prothrombin and homozygous methylenetetrahydrofolate reductase gene mutations were significantly more prevalent than in the controls. Thrombophilic patients with severe preeclampsia are at increased risk of acute renal failure (OR, 1.8; 95% CI, 1.5 to 2.2), disseminated intravascular coagulation (OR, 2.7; 95% CI, 1.1 to 6.4), abruptio placentae (OR, 2.6; 95% CI, 1.2 to 6.0) and perinatal mortality (OR, 1.7; 95% CI, 1.5 to 2.2) compared with nonthrombophilic preeclamptic patients. Our study demonstrates a significant association between maternal thrombophilia and severe preeclampsia in white women. Thrombophilia also augments the risk of life-threatening maternal complications and adverse perinatal outcomes in preeclamptic patients.
Hypertension 2005 Dec
PMID:Thrombophilia is significantly associated with severe preeclampsia: results of a large-scale, case-controlled study. 1628 82

Hemostatic changes might contribute to the increased risk of cardiovascular and cerebrovascular events in patients with obstructive sleep apnea (OSA). We investigated the effect of a short-term isocapnic hypoxic challenge on coagulation activation markers thrombin/antithrombin III complexes (TAT) and D-dimer in OSA. Thirty-two OSA patients (mean age 48 +/- 11 years) inhaled a gas mixture containing 10% O(2) and 90% N(2) and further adjusted to yield pulse oximetry saturation of 80-85% for 5 minutes. Plasma levels of TAT and D-dimer were measured immediately before and immediately after the hypoxic challenge. The hypoxic challenge provoked a significant increase in TAT (p < 0.001) and in D-dimer (p = 0.037). Mean nocturnal oxygen saturation from the sleep recordings correlated with D-dimer increase (r = -0.37, p = 0.041). Also, OSA patients with a history of hypertensive parents had greater D-dimer increase in response to hypoxia than patients having normotensive parents (p = 0.035). Parental hypertension independently explained 15% of the variance in D-dimer increase after hypoxia (p = 0.035). Oxygen desaturation during sleep may predispose OSA patients, in particular those with a parental history of hypertension, to a hypercoagulable state providing one explanation for the increased risk of atherothrombotic events in this population.
...
PMID:Short-term isocapnic hypoxia and coagulation activation in patients with sleep apnea. 1631 46

According to current concepts, hypertension and hyperlipidemia cause vascular damage that leads to a hypercoagulative state. In this study, we investigated whether spontaneously hypertensive and hyperlipidemic rats (SHHR) can be a useful experimental model for complications in combined hypertension and hyperlipidemia, by comparing coagulative and fibrinolytic activities in SHHR with those in spontaneously hypertensive rats (SHR) and spontaneously hyperlipidemic rats (HLR). We measured coagulation and fibrinolysis markers in plasma and levels of fibrinogen and prothrombin mRNA in livers of eight-month-old male Wistar Kyoto rats (WKY), Sprague-Dawley rats (SD), SHR, HLR and SHHR. The plasma levels of fibrinogen in SHR, HLR and SHHR were significantly higher than those in WKY and SD, and were highest in SHHR. Higher plasma levels of antithrombin III and plasminogen were detected in increasing order in SHR, HLR and SHHR as compared to those in WKY and SD. Hepatic mRNA expressions of fibrinogen chains and prothrombin were enhanced in SHR, HLR and SHHR, resulting in increased plasma fibrinogen levels in SHHR. These results suggest that hypertension and hyperlipidemia can each cause hypercoagulation, with hyperlipidemia being a stronger factor than hypertension. Since a greater hypercoagulative state is a complication of combined hypertension and hyperlipidemia, the SHHR model is a good system for studying the early stage of atherosclerosis ensuing from hyperfibrinogenemia.
...
PMID:Development of hyperfibrinogenemia in spontaneously hypertensive and hyperlipidemic rats: a potentially useful animal model as a complication of hypertension and hyperlipidemia. 1728 85

A 38-year-old male Caucasian with Fabry disease presented with angiokeratomas and tortuous conjunctival and retinal vessels. Additionally, the patient showed characteristic skin lesions of psoriasis and seborrheic dermatitis. His past medical history revealed anhidrosis, acral paresthesias, myocardial infarction, phlebothrombosis, hypertension, antithrombin III deficiency, factor V Leiden disease, chronic obstructive lung disease, tinnitus, diarrhea, recurrent abdominal pain, headache, and depressive mood. He was treated with intravenous substitution of the deficient enzyme alpha-galactosidase A. Possible future options in treatment of Fabry disease are discussed.
...
PMID:Fabry disease: case report with emphasis on enzyme replacement therapy and possible future therapeutic options. 1761 Jun 10


<< Previous 1 2 3 4 5 6 7 8 9 10

---