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

Plasma levels of tumor markers (CEA, TPA, CA 15.3, CA 125, alpha-fetoprotein) for 50 patients with hypertensive disorders of pregnancy were compared with those of 50 healthy women with singleton pregnancies and 50 healthy non-pregnant controls. With the exception of CEA all tumor marker values were higher in pregnant women, these differences being statistically significant (all p < 0.0001). Alpha-fetoprotein was lower in hypertensive than in healthy pregnant women (p = 0.0004), whereas CEA, CA 15.3 and CA 125 showed no statistically significant differences. TPA values in patients with hypertensive disorders of pregnancy (median 190 U/l) were 2.7 times higher than those of healthy pregnant controls (median 70.5 U/l) with a statistically significant difference (p < 0.0001). The individual degrees of disease severity demonstrated increasing TPA medians (pregnancy-induced hypertension: 106.5 U/l; pre-eclampsia: 200 U/l; HELLP syndrome: 339 U/l). TPA levels correlated positively with clinical severity of disease and negatively with fetal (rs = -0.58; p < 0.0001) and placental weight (rs = 0.44; p = 0.01).
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PMID:Tumor markers in hypertensive disorders of pregnancy. 768 29

A large number of ascitic fluid tests, e.g., fibronectin and cholesterol, have been proposed as helpful in detecting malignancy as the cause of ascites. Unfortunately, these "humoral tests of malignancy" are nonspecific. Although the ascitic fluid concentrations of these proteins or protein-bound substances tend to be quite high in patients with peritoneal carcinomatosis and low in the setting of cirrhotic ascites, the problem is that patients with tuberculous peritonitis, cardiac ascites, pancreatitis ascites, etc. usually have values in the malignancy range, i.e., false-positive results. This can lead to an extensive search for a nonexistent tumor, with confusion and anxiety for patient and physician. The cytology is the single best test to order when peritoneal carcinomatosis is suspected; its sensitivity approaches 100%. However, peritoneal carcinomatosis is only one of several mechanisms by which tumors can cause ascites. No one test can be expected to detect tumors as the cause of these diverse mechanisms of ascites formation. The serum-ascites albumin gradient is a helpful test in classifying ascitic fluid specimens into portal-hypertension-related and non-portal-hypertension-related categories. An elevated serum alpha-fetoprotein test can be useful in raising suspicion of hepatocellular carcinoma. Careful analysis of ascitic fluid, without measurement of "humoral tests of malignancy," combined with information obtained from the history and physical examination, usually lead to an accurate diagnosis of the cause of ascites.
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PMID:Malignancy-related ascites and ascitic fluid "humoral tests of malignancy". 818 30

To evaluate the variations and potential clinical use of serial maternal alpha-fetoprotein (AFP) and human chorionic gonadotropin (hCG) in pregnancies at risk of pregnancy-induced hypertension (PIH) and/or intrauterine growth retardation (IUGR), we investigated the relationship between placental sonographic findings, uterine artery Doppler measurements, and maternal serum AFP, hCG, and uric acid levels between 20 and 34 weeks of pregnancy. Maternal serum samples were collected from 41 singleton pregnancies with bilateral uterine notches and/or an increased uterine artery pulsatility index at 20-24 weeks. Maternal serum AFP, intact hCG and free alpha and beta subunits, and uric acid circulating levels were measured in all cases at 20-24 weeks and 25-28 weeks. Placental sonographic investigations comprised measurements of thickness and morphology. Twenty pregnancies had a normal outcome and 21 had an adverse outcome, including eight complicated by severe PIH with fetal IUGR, eight by isolated IUGR, three by mild PIH with normal fetal growth, and two by placental abruption. At the time of the first scan, the placental thickness and maternal serum levels of AFP, hCG, and uric acid were significantly increased in pregnancies with adverse outcomes, compared with those with a normal outcome. In subsequent maternal serum examinations, the incidence of elevated hormonal levels fell for AFP, intact hCG, and beta-hCG, whereas it increased for the uric acid level. No difference was found at any stage for the alpha-hCG level. Seven out of 11 pregnancies complicated by PIH presented with elevated MSAFP and MShCG and a large heterogeneous placenta at the first visit, whereas no pregnancy with a normal outcome presented with similar features. This study has shown a significant association between abnormal development of the utero-placental circulation, elevated MSAFP and MShCG at mid-gestation, and subsequent adverse pregnancy outcome. Serial measurements of MSAFP and MShCG do not provide extra information for the follow-up of these pregnancies.
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PMID:Maternal serum testing for alpha-fetoprotein and human chorionic gonadotropin in high-risk pregnancies. 899 49

From Antenatal Diagnostic Center referrals over 22 months, consultations for early-onset fetal growth restriction versus skeletal dysplasia were retrospectively identified. Those with elevated maternal serum alpha-fetoprotein (MSAFP) levels are the focus of this report. All had an early ultrasound confirming menstrual dates and subsequent sonography at < 28 weeks with at least two fetal biometric measures delayed by > or = 2 standard deviations from mean values. Of the five patients identified, the mean gestational age at the time of diagnosis of fetal growth restriction was 23.3 +/- 2.9 weeks. All had normal karyotypes and normal amniotic fluid AFP. None of the patients had evidence of hypertension or pre-eclampsia at diagnosis of fetal growth restriction. All five gravidas subsequently developed severe pre-eclampsia from 5.5 to 12.5 weeks after documentation of fetal growth delay. Three developed HELLP syndrome. Pregnancies were continued a mean duration of 10-2 weeks, with all five delivering at preterm gestations (mean = 33.5 +/- 1.7 weeks) for maternal indications of severe pre-eclampsia. Unexplained early-onset fetal growth restriction in conjunction with unexplained elevations of MSAFP together consistently heralded the subsequent development of severe pre-eclampsia.
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PMID:The association of early-onset fetal growth restriction, elevated maternal serum alpha-fetoprotein, and the development of severe pre-eclampsia. 916 Mar 81

Unexplained elevated or low maternal serum alpha-fetoprotein (MSAFP) is reported to indicate adverse perinatal outcome. We designed a prospective matched pair study to gain additional information about the type and frequency of adverse neonatal or maternal outcomes. Subjects were selected from 16,445 women who received second trimester MSAFP screening during the 4.5 year study period. For each unexplained elevated or low subject, a control patient in the second trimester of pregnancy was chosen by matching eight individual traits. After follow-up, 356 pairs were identified, for the unexplained low MSAFP group and 139 pairs for the unexplained elevated MSAFP group. Outcome information was obtained by way of a physician questionnaire. For the unexplained low MSAFP group, complications occurred no more often than for the paired controls and these pregnancies may not be considered at high risk for adverse outcome. Our study supports a strong association between unexplained elevated MSAFP and adverse neonatal outcomes of low birth weight, fetal death, preterm delivery, and fetal growth retardation. The highest frequency of adverse neonatal outcome occurred when the multiple of median value was > or = 4.0. Our study does not support an association between elevated MSAFP and maternal complications of hypertensive disorder, oligohydramnios, or placental abruption.
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PMID:Perinatal outcomes in a prospective matched pair study of pregnancy and unexplained elevated or low AFP screening. 949 19

We wanted to study if maternal serum mid-trimester total renin, inhibin A, AFP or free beta-hCG levels predict the development of pre-eclampsia. Maternal serum alpha-fetoprotein (AFP) and human chorion gonadotrophin (beta-hCG) were evaluated in the screening programme for Down syndrome in 4356 patients prospectively. Data on pregnancy outcome were available in 1242 women. Pregnancy-induced hypertension (PIH) developed in 69 women, 282 women with uneventful pregnancy outcome were selected for controls. Serum total renin and inhibin A levels were measured retrospectively in the trisomy screening samples of 69 and 30 patients who later developed PIH, and in 282 and 7 patients, respectively, who had an uneventful pregnancy outcome. No significant differences were found in the levels of maternal mid-trimester serum total renin, inhibin A or free beta-hCG levels between PIH and healthy women. The multiples of the median (MoM) of AFP values were significantly higher in the subgroup of patients who later developed severe pre-eclampsia than in patients with mild pre-eclampsia or gestational hypertension and healthy pregnant women. Maternal mid-trimester serum levels of total renin, inhibin A and free beta-hCG are not predictive for development of PIH. High mid-trimester serum AFP values may help in the prediction of severe pre-eclampsia.
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PMID:Prediction of pre-eclampsia with maternal mid-trimester total renin, inhibin A, AFP and free beta-hCG levels. 1021 68

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

Data from a nested case-control study were analyzed to examine high mean arterial pressure (MAP), hypertension of pregnancy, and preeclampsia as independent predictors and as surrogate markers for elevated alpha-fetoprotein (AFP) levels in evaluating breast cancer risk. Cases (n = 205) were identified by the California Cancer Registry from a cohort of pregnant women who were part of the Kaiser Health Plan and took part in the Child Health and Development Studies initiated by the University of California, Berkeley, from June 1959 to September 1966. Controls (n = 337) were selected by randomized recruitment from the same cohort probability matched to cases by distribution of birth dates of cases. High MAP was associated with breast cancer risk and is different across quartile of age at first full-term pregnancy as is high AFP. Odds ratios (OR) across quartiles for MAP were 0.24 [95% confidence interval (CI), 0.08-0.71], 0.84 (95% CI, 0.39-1.66), 1.00 (referent), and 2.50 (95% CI, 1.21-5.13), and for AFP were 0.34 (95% CI, 0.13-0.93), 0.77 (95% CI, 0.36-1.67), 1.00 (referent), and 2.38 (95% CI, 1.13-5.00). Neither diagnosed preeclampsia nor hypertension of pregnancy showed any association with breast cancer risk. When both high AFP and high MAP were entered into the same analysis, neither changed the OR for the other more than 8%. Additionally, AFP level was not a linear function of MAP. Although the pattern of ORs across quartiles of age at first full-term pregnancy was similar for the two variables, it cannot be concluded that high MAP is an adequate surrogate for high levels of maternal serum AFP, but rather represents some related process that is in and of itself a risk factor for breast cancer.
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PMID:Mean arterial pressure, pregnancy-induced hypertension, and preeclampsia: evaluation as independent risk factors and as surrogates for high maternal serum alpha-fetoprotein in estimating breast cancer risk. 1114 21

Oxidized low density lipoproteins (oxLDL) formed in vivo induce a humoral immune response. Oxidative modification of LDL renders it immunogenic and a heterogeneous population of specific anti-oxLDL antibodies is produced. These antibodies could represent a biological marker of oxidative stress and serve as markers of atherosclerosis. Autoantibodies against oxLDL (oLAb) have been detected in human subjects practically of every age. oLAb also appear in the blood of pregnant women. Some studies have shown that the levels of antibodies to oxLDL were elevated in women with established preeclampsia. The present study was aimed to estimate the oLAb IgG levels in the first and second trimester of pregnancy. Furthermore, we estimated the correlation between maternal serum (MS) levels of oLAb and alpha-1-fetoprotein (MS AFP), human chorionic gonadotrophin (MS HCG) and trophoblast-specific-beta-1-glycoprotein (MS SP1), because these proteins are determined as a part of prenatal biochemical screening for fetal congenital abnormalities. Our study deals with the oLAb changes in women with pregnancy-induced hypertension. We also investigated the correlation between oLAb IgG and anticardiolipin antibodies IgG (ACA) in the serum of pregnant women. We examined 40 pregnant women attending Institute for Mother and Child Care for their antenatal care as outpatients. Routine blood samplings between the 9-13th week of pregnancy and 16-18th week of pregnancy were performed as a part of biochemical prenatal screening for fetal congenital abnormalities (Group 1). Their mean age was 27 +/- 4.1 years. Furthermore, we examined 26 women in the second or third trimester with pregnancy-induced hypertension (Group 2). Group 2 was compared with 49 pregnant women in the second or third trimester who were normotensive (Group 3). We used commercial standardized ELISA kits for determination of oLAb IgG, ACA IgG, MS AFP and MS HCG, MS SP1 was analyzed by single radial immunodiffusion. We did not find any differences in the levels of oLAb IgG in the first and second trimester in the women of Group 1. The correlation between oLAb and ACA IgG was not statistically significant (Spearman coefficient r=0.22, p=0.1). The correlation between oLAb IgG with MS AFP, MS HCG and MS SP1 was not statistically significant. Weak negative correlation for AFP and HCG was suggested both in the first and in the second trimester. The levels of oLAb IgG in the group of women with pregnancy-induced hypertension were significantly lower than in the group of normotensive women (348 +/- 388 U/ml v.s. 579 +/- 400 mU/ml, p<0.01). We can conclude that the levels of oLAb do not differ in the first and second trimester of gravidity. However, we cannot exclude the possible influence of an inverse relationship between oLAb IgG titers and the synthesis of fetoplacental antigens. This finding is important especially in the context of the results of prenatal biochemical screening. Pregnancy-induced hypertension is associated with lower levels of oLAb. Weak cross-reactivity between oLAb and anticardiolipin antibodies may exist but there is a possibility that there are two different populations of antibodies reacting with various antigens.
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PMID:Antibodies against oxidized low density lipoproteins in pregnant women. 1244 33

In a prospective, blind study of 183 unselected women attending for routine booking scan with a singleton pregnancy at 16-24 weeks' gestation, uteroplacental resistance index, and peripheral levels of alpha-fetoprotein, human chorionic gonadotropin, human placental lactogen, Schwangerswaft protein, pregnancy-associated placental protein A and insulin-like growth factor (IGF) binding protein 1 were measured. High levels of alpha-fetoprotein and IGF 1 binding protein 1 (> 90th centile) were associated with small-for-gestational age babies (< 10th centile) (sensitivity 24% and 22%; specificity 90% and 91%). High levels of alpha-fetoprotein, human chorionic gonadotropin and pregnancy-associated placental protein A (> 90th centile) were associated with one or more of three severe complications of pregnancy: very small-for-gestational age (< 3rd centile), severe proteinuric hypertension or intrauterine death (sensitivity 20%, 20% and 57%; specificity 90%, 95% and 91%, respectively). A uteroplacental resistance index > 90th centile was also associated with small-for-gestational age and severe complications (sensitivity 24% and 50%, specificity 90% and 90%). A combination of resistance index and a placental function test improved the prediction for a group of patients that included any complications (sensitivity 31% and specificity 89%). Doppler ultrasound was a more efficient predictor than individual placental function tests but screening predictions can be improved by combining Doppler parameters and placental protein estimations. Combinations of placental function tests might provide equivalent, or complementary, information. This preliminary work demonstrates the potential value of combining biophysical and biochemical tests to predict complications of pregnancy.
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PMID:Early prediction of uteroplacental complications of pregnancy using Doppler ultrasound, placental function tests and combination testing. 1279 32


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