Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of preeclampsia is unknown. At present, 4 hypotheses are the subject of extensive investigation, as follows: (1) Placental ischemia-Increased trophoblast deportation, as a consequence of ischemia, may inflict endothelial cell dysfunction. (2) Very low-density lipoprotein versus toxicity-preventing activity-In compensation for increased energy demand during pregnancy, nonesterified fatty acids are mobilized. In women with low albumin concentrations, transporting extra nonesterified fatty acids from adipose tissues to the liver is likely to reduce albumin's antitoxic activity to a point at which very-low density lipoprotein toxicity is expressed. (3) Immune maladaptation-Interaction between decidual leukocytes and invading cytotrophoblast cells is essential for normal trophoblast invasion and development. Immune maladaptation may cause shallow invasion of spiral arteries by endovascular cytotrophoblast cells and endothelial cell dysfunction mediated by an increased decidual release of cytokines, proteolytic enzymes, and free radical species. (4) Genetic imprinting-Development of preeclampsia-eclampsia may be based on a single recessive gene or a dominant gene with incomplete penetrance. Penetrance may be dependent on fetal genotype. The possibility of genetic imprinting should be considered in future genetic investigations of preeclampsia.
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PMID:Etiology and pathogenesis of preeclampsia: current concepts. 1052 45

The endothelins (ETs) are regulatory peptides, distributed in many organ systems and producing potent physiological effects. They are the most powerful vasoconstrictive substances known today. They also act as promitogens. Many data supporting pathophysiological roles for ETs are reported, especially regarding diseases related to the vascular system, such as hypertension, pulmonary hypertension, preeclampsia, ischemic heart diseases, renal failure, subarachnoidal hemorrhage, and cerebral ischemia. The development of drugs blocking ET binding to its receptors (antagonists) and the biosynthesis of ETs (ECE inhibitors) presently attracts great interest in terms of establishing new treatments for diseases in which ETs are believed to be involved. Here we review the evidence supporting a role for ETs in the various etiologies related to ischemia-reperfusion injury, such as is found in heart disease, cerebral ischemia, and organ transplantation.
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PMID:The many aspects of endothelins in ischemia-reperfusion injury: emergence of a key mediator. 982 48

The HELLP syndrome is a dangerously severe form of preeclampsia associated with multiorgan system damage and occurs in 0.2-0.6% of all pregnancies. It usually presents with abdominal pain, often in the setting of preeclampsia. In most cases, HELLP is initiated by inadequate placental vessel development with subsequent placental ischemia, leading to the release of circulating vasoconstrictors. These powerful vasoconstrictors include thromboxane A2, angiotensin, prostaglandin F2, and endothelin-1. The ischemic placenta also produces fewer vasodilators, such as prostacyclin, prostaglandin, E2, and nitric oxide. The ensuing imbalance in vasoactive substances causes intense systemic vasospasm and multiorgan endothelial damage. Multiple genetic, coagulation, and immunologic disorders also appear to contribute to the endothelial damage. Fibrin and platelets are then deposited on the endothelial surfaces leading to the hemolytic anemia, elevated liver enzymes, and low platelets of the HELLP syndrome. The most reliable laboratory tests for the diagnosis of HELLP are a complete blood count with peripheral smear, lactate dehydrogenase, serum transaminases, and urinalysis. Supportive tests include serum haptoglobin, D-dimer fragment levels, lactate dehydrogenase isoenzymes, total bilirubin, prothrombin times, and activated partial thromboplastin times. Lactate dehydrogenase and the platelet count are the two best tests to monitor the course of the disease. Prompt delivery is the treatment of choice. The intensity of the HELLP syndrome peaks 24 hours after delivery. Extended atypical HELLP has been successfully treated with plasma exchange. The clinical laboratory professional plays an important role in the diagnosis, follow-up, and treatment of patients with the HELLP syndrome.
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PMID:HELLP! A cry for laboratory assistance: a comprehensive review of the HELLP syndrome highlighting the role of the laboratory. 984 23

Some of the maternal symptoms of preeclampsia can be produced by uterine ischemia, although no quadriped spontaneously exhibits this disease. It may be that the combination of upright posture and uteroplacental ischemia are necessary for manifestation of the full syndrome. Chronic nitric oxide synthase inhibition in rats produces a pattern of change that resembles the symptoms of preeclampsia, and the preeclamptic-like response of rats with adriamycin nephropathy and hyperinsulinemia is associated with endothelial dysfunction. These models are definitely of use in preeclampsia research, but because this disease only occurs spontaneously in primates, the definitive studies on preeclampsia will, of necessity, be clinical.
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PMID:Animal models of preeclampsia. 1010 66

The immune maladaptation hypothesis of preeclampsia is concordant with cytokine-mediated oxidative stress, chronology of endothelial activation, lipid changes, adverse effect of changing partners, and the protective effect of sperm exposure. Genetic factors may involve underlying hereditary thrombophilic disorders and hyperhomocysteinemia, essential hypertension and/or obesity, or control of the Th1/Th2 balance and thus affect the maternal response against fetal antigens. Placental ischemia and increased syncytiotrophoblast deportation are probably end-stage disease phenomena.
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PMID:The immunology of preeclampsia. 1010 68

The pathogenesis of atheromatous and/or thrombotic vascular diseases involves rheological parameters, soluble mediators and cellular agents. The many studies that have tried to establish correlations between plasma factors, shear stress and the risk of ischemia have left some questions unanswered. Current exploration methods are now focusing on the determining role of cells. Activated cells express adhesion molecules on their membranes, which allow to communicate in a homo- or heterotypical manner. Quantifying adherence molecules on the surface of platelets, leukocytes and endothelial cells provides an assessment of the "adhesive phenotypical profile". Quantitative cytometry, using beads coated with a known amount of immunoglobulins as calibrators, is perfectly suited, through its multiple parameter analyses and the specificity provided by monoclonal antibodies, for the quantification of membrane antigens. Measuring the adhesive profile on the surface of cells that are implicated in vascular disease makes it possible to correlate that phenotype to the ischemic risk in such diversified pathologies or circumstances as intermittent angor, myocardial infarction, angioplasty, insulin-dependent diabetes or pre-eclampsia. In addition, that quantification permits monitoring the action of new therapeutical agents targeting adherence molecules.
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PMID:[Vascular disease and cellular activation: exploration of cell adhesion phenotype by quantitative flow cytometry]. 1019 30

High blood pressure during pregnancy (BP > or = 140/90 mmHg) is sometimes already noted before conception, with usually a good prognosis (although it could predispose to preeclampsia). alpha-methyldopa is the best treatment when needed (agents blocking the renin angiotensin system are not recommended). Preeclampsia, a form of hypertension noted after 20 weeks of gestation with proteinuria is a more serious condition (BP > or = 140/90 mmHg or increase in BP from the 1st trimester > or = 25/15 mmHg). It is generated by placental ischemia and creates maternal endothelial lesions which in turn decrease the blood flow to placenta leading to maternal and fetal syndromes. Hospitalisation is mandatory. No measure other than delivery is known to attenuate or reverse its progression. Treating hypertension during pregnancy (when blood pressure > or = 170/110 mmHg) aims at preventing maternal risk (stroke or eclampsia) but has few effect on foetal lesions. Prevention of this syndrome, which represents the first secondary cause of hypertension, is until now disappointing.
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PMID:[Hypertension at pregnancy]. 1039 40

Whole blood flow cytometry is a powerful new laboratory technique for assessment of platelet activation and function. Flow cytometry can be used to measure platelet hyperreactivity, circulating activated platelets, leukocyte-platelet aggregates, and procoagulant platelet-derived microparticles in a number of clinical settings, including acute coronary syndromes, angioplasty, cardiopulmonary bypass, acute cerebrovascular ischemia, peripheral vascular disease, diabetes mellitus, preeclampsia, and Alzheimer's disease. Clinical applications of whole blood flow cytometric assays of platelet function in these diseases may include identification of patients who would benefit from additional antiplatelet therapy and prediction of ischemic events. Circulating monocyte-platelet aggregates appear to be a more sensitive marker of in vivo platelet activation than circulating P-selectin-positive platelets. Flow cytometry can also be used in the following clinical settings: monitoring of glycoprotein IIb-IIIa antagonist therapy, diagnosis of inherited deficiencies of platelet surface glycoproteins, diagnosis of storage pool disease, diagnosis of heparin-induced thrombocytopenia, and measurement of the rate of thrombopoiesis.
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PMID:Laboratory markers of platelet activation and their clinical significance. 1046 51

The pathogenesis of cortical blindness as a rare complication in severe preeclampsia is still unclear. The case of a women with postpartum blindness is reported in which CT and MRI initially showed cortical and subcortical edema in the parieto-occipital lobes. At this time cerebral angiography and transcranial color-coded sonography (TCCS) revealed widespread cerebral vasospasm. Mean blood flow velocities in the middle and posterior cerebral artery and carotid syphon initially reached 380 cm/s and normalized within 2 weeks. While the patient's vision improved rapidly, follow-up MRI disclosed ischemic lesions and petechial hemorrhage in the occipital cortex. This case provides rare documentation that transient blindness in patients with preeclampsia may result from parieto-occipital ischemia due to cerebral vasospasm. In such patients TCCS may be useful to detect vasospasm associated with preeclampsia/eclampsia.
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PMID:[Transient cortical blindness in EPH gestosis caused by cerebral vasospasm]. 1055 88

Retinal detachment is an unusual complication of hypertensive disorder in pregnancy. It has been reported in 1% to 2% of patients with severe preeclampsia and in 10% of patients with eclampsia. Choroidal ischemia may be the cause of retinal detachment. We know that mild arteriolar spasm involving the bulbar conjunctival vessels has been observed in the normal pregnancy, but in pregnancy-induced hypertension the vasospasm may be severe and result in choroidal ischemia. Most patients with retinal detachment in pregnancy-induced hypertension have had full spontaneous resolution within a few weeks, and they did not have any sequelae. Medical treatment with antihypertensive drugs and steroids may be helpful. We report two rare cases of retinal detachment and persistent hypertension in association with postpartum eclampsia and post-cesarean section preeclampsia. These patients had normotension throughout pregnancy. Preeclampsia or eclampsia developed after delivery, and blurred vision, headache, and reduced vision accompanied serous retinal detachment. The serous retinal detachment disappeared within 3 weeks. Good outcomes were found in the follow-up examinations in both of these cases. For women who had been normotensive at the time of delivery and then complained in the postpartum period of blurred vision, headaches, nausea and vomiting, we should consider the possibility of retinal detachment and perform fundoscopy.
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PMID:Retinal detachment in postpartum preeclampsia and eclampsia: report of two cases. 1058 29


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