Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcemia is a common paraneoplastic syndrome that may result in metastatic calcification. We report here on four autopsy cases with paraneoplastic hypercalcemia with metastatic calcification, to evaluate the clinicopathologic manifestations. All were males, aged 37-63 years old. Primary tumors included one transitional cell carcinoma of the urinary bladder, one multiple myeloma, and two squamous cell carcinomas of the esophagus. Calcium concentrations ranged from 3.3 to 5.9 mmol/L. Chronic hypercalcemia resulted in metastatic calcification. The kidney and stomach were the most vulnerable organs. Only case 1 presented with an increase in plasma calcium above 5 mmol/L (about twice the normal value); the metastatic calcification involved the capillary walls of his lungs, and he died of fulminant pulmonary edema. Our conclusion is that judicious treatment for paraneoplastic hypercalcemia is important with respect to the occurrence of pulmonary edema associated with metastatic calcification.
 ...
PMID:Paraneoplastic hypercalcemia with metastatic calcification--clinicopathologic studies. 1656 25

Ion transport is essential for maintenance of transmembranous and transcellular electric potential, fluid transport and cellular volume. Disturbance of ion transport has been associated with cellular dysfunction, intra and extracellular edema and abnormalities of epithelial surface liquid volume. There is increasing evidence that conditions characterized by an intense local or systemic inflammatory response are associated with abnormal ion transport. This abnormal ion transport has been involved in the pathogenesis of conditions like hypovolemia due to fluid losses, hyponatremia and hypokalemia in diarrhoeal diseases, electrolyte abnormalities in pyelonephritis of early infancy, septicemia induced pulmonary edema, and in hypersecretion and edema induced by inflammatory reactions of the mucosa of the upper respiratory tract. Components of membranous ion transport systems, which have been shown to undergo a change in function during an inflammatory response include the sodium potassium ATPase, the epithelial sodium channel, the Cystic Fibrosis Transmembrane Conductance Regulator and calcium activated chloride channels and the sodium potassium chloride co-transporter. Inflammatory mediators, which influence ion transport are tumor necrosis factor, gamma interferon, interleukins, transforming growth factor, leukotrienes and bradykinin. They trigger the release of specific messengers like prostaglandins, nitric oxide and histamine which alter ion transport system function through specific receptors, intracellular second messengers and protein kinases. This review summarizes data on in vivo measurements of changes in ion transport in acute inflammatory conditions and in vitro studies, which have explored the underlying mechanisms. Potential interventions directed at a correction of the observed abnormalities are discussed.
 ...
PMID:Changes in ion transport in inflammatory disease. 1657 Nov 16

Spontaneous preterm labour and delivery accounts for approximately one-third of preterm births, which is the predominant cause of perinatal mortality and morbidity. This review aims to evaluate the evidence on the benefits and harms of five classes of tocolytic therapy, namely: betamimetics, calcium channel blockers, magnesium, non-steroidal anti-inflammatory agents, and atosiban. We performed a systematic review of the effectiveness of tocolytics to stop uterine contractions (first-line therapy). Reports of randomised controlled trials from searches of MEDLINE, bibliographies of review articles, Cochrane Collaboration and its Pregnancy and Childbirth Review Group between 1966 and 2003 were identified, using the search terms "randomised controlled trial" (RCT), "preterm labor", "tocolysis", "betamimetics", "ritodrine", "prostaglandin synthetase inhibitors", "indomethacin", "calcium channel blockers", "nifedipine", "oxytocin receptor blockers", "atosiban", and "magnesium sulphate". Studies on women with preterm labour comparing the effects of a tocolytic with a placebo or no treatment that met our inclusion criteria, were included. To our knowledge, the trials were conducted mainly before 1999 and there were no placebo-controlled trials after that. Of the 86 articles identified and evaluated, 14 first-line studies met more stringent requirements for meta-analyses. Tocolytics were associated with significant decreases in the odds of delivery within 24 hours (odds-ratio [OR] 0.54, 95 percent confidence interval [CI] 0.32-0.91) and 48 hours (OR 0.47, 95 percent CI 0.30-0.75). These effects were significant for beta-agonists, atosiban and indomethacin, but not magnesium sulphate. Maternal side-effects significantly associated with betamimetics were pulmonary oedema, cardiac arrhthymias and hypokalaemia. Although calcium antagonists have not been evaluated against placebo, comparative trials with beta-agonists have shown more favourable neonatal outcomes and better prolongation of gestation. In conclusion, the management of threatened preterm labour with first-line tocolytic therapy can prolong gestation. However, the time gained in-utero need to be optimised. There is no clear first-line tocolytic agent. The use of tocolytic agents should be individualised and based on maternal condition, potential side-effects and gestational age.
 ...
PMID:Tocolytic treatment for the management of preterm labour: a systematic review. 1664 83

We report the case of attempted suicide with amlodipine, chlorthalidone and mefenamic acid and subsequent medical intensive care measures which resulted in total recovery of a 42-year-old male. After admission to the medical intensive care unit the intoxicated patient was deeply hypotensive and needed fluid replacement, dobutamine and norepinephrine. Additionally insulin and calcium gluconate were given. Since hypotension persisted and the patient developed oliguria, terlipressin was applied and finally showed an effect on blood pressure and on urinary output. A volume overload of 7 L in the first 24 h resulted in a pulmonary edema. The patient was started on non-invasive ventilation with continuous positive airway pressure (CPAP) and frusemide was added to the therapy with good success. Quantitative determination of amlodipine in plasma samples was performed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The highest amlodipine concentrations was measured in the plasma sample collected approximately 8 h after ingestion of the drug, and was 393 microg/L. Four days later, it was possible to stop the treatment with catecholamines, at that time the amlodipine plasma concentration had declined to 132 microg/L, still tenfold higher than therapeutic (5-18 microg/L). Elimination half-life of amlodipine is approximately 55 h. After 6 days in the intensive care unit the patient was transferred to psychiatric treatment. Intensive care management and plasma levels in this intoxication case are compared to data from literature on other cases.
 ...
PMID:Survival of severe amlodipine intoxication due to medical intensive care. 1687 74

Hypertension promotes left ventricular (LV) hypertrophy and myocardial remodeling and is frequently present in patients with systolic or diastolic heart failure. Control of hypertension in both of these settings may attenuate progressive LV hypertrophy and remodeling and improve clinical outcomes. Guidelines for the management of heart failure recommend that hypertension should be treated in all patients with preclinical heart failure as well as in those with heart failure with reduced or preserved LV systolic function. Consistent with national hypertension guidelines, the goal for blood pressure control in hypertensive patients with heart failure is less than 140/90 mm Hg, but lower targets (< 130/80 mm Hg) may be desirable in those with concomitant diabetes mellitus or renal disease. Angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, and beta-adrenoreceptor antagonists are first-line options for hypertension treatment in heart failure. Calcium channel antagonists and the alpha blocker doxazosin should be avoided. Episodes of recurrent pulmonary edema and hypertension may also indicate underlying severe renovascular disease that may respond to percutaneous renal artery intervention.
 ...
PMID:Goals and guidelines for treating hypertension in a patient with heart failure. 1703 73

Preterm birth is never low risk and there are advantages gained by prolonging gestation even at relatively advanced stages of pregnancy. This means that high-value treatments should not just be reserved for high-risk pregnancies. Some women treated with tocolytics will experience adverse events, and some adverse events are particularly associated with different classes of tocolytic agents. Cardiovascular adverse events are particularly common with beta-agonists and there have been several maternal deaths from pulmonary oedema as a result of beta-agonist use for tocolysis. Calcium channel blockers are often associated with maternal hypotension, and a number of case studies reporting serious adverse events have been reported. The aim of this case study is to discuss what can be done if a patient experiences adverse events with tocolytics, and suggests approaches to continuing patient management and implications for obstetric practice.
 ...
PMID:'Normal' pregnancy with adverse events on initial tocolytic treatment. 1720 79

Hypoxic pulmonary vasoconstriction (HPV) occurs with ascent to high altitude and can contribute to development of high altitude pulmonary edema (HAPE). Vascular smooth muscle contains carbonic anhydrase (CA), and acetazolamide (AZ), a CA inhibitor, blunts HPV and might be useful in the prevention of HAPE. The mechanism by which AZ impairs HPV is uncertain. Originally developed as a diuretic, AZ also has direct effects on systemic vascular smooth muscle, including modulation of pH and membrane potential; however, the effect of AZ on pulmonary arterial smooth muscle cells (PASMCs) is unknown. Since HPV requires Ca2+ influx into PASMCs and can be modulated by pH, we hypothesized that AZ alters hypoxia-induced changes in PASMC intracellular pH (pH(i)) or Ca2+ concentration ([Ca2+](i)). Using fluorescent microscopy, we tested the effect of AZ as well as two other potent CA inhibitors, benzolamide and ethoxzolamide, which exhibit low and high membrane permeability, respectively, on hypoxia-induced responses in PASMCs. Hypoxia caused a significant increase in [Ca2+](i) but no change in pH(i). All three CA inhibitors slightly decreased basal pH(i), but only AZ caused a concentration-dependent decrease in the [Ca2+](i) response to hypoxia. AZ had no effect on the KCl-induced increase in [Ca2+](i) or membrane potential. N-methyl-AZ, a synthesized compound lacking the unsubstituted sulfonamide group required for CA inhibition, had no effect on pH(i) but inhibited hypoxia-induced Ca2+ responses. These results suggest that AZ attenuates HPV by selectively inhibiting hypoxia-induced Ca2+ responses via a mechanism independent of CA inhibition, changes in pH(i), or membrane potential.
 ...
PMID:Inhibition of hypoxia-induced calcium responses in pulmonary arterial smooth muscle by acetazolamide is independent of carbonic anhydrase inhibition. 1720 36

Calcium channel blockers of the dihydropyridin's family have been associated with the onset of an acute pulmonary edema when they are used as a treatment of preterm labor. We report here four cases of pulmonary edema in pregnant women treated with nicardipine (Loxen) for preterm labor. The physiopathology of pulmonary edema, the pharmacology of calcium channel blockers of dihydropyridin's family and the detailed analysis of our cases and those of the literature make us discuss of the role of these agents and associated population and risk factors in such complication.
 ...
PMID:[Pulmonary edema during calcium-channel blockers therapy: role of predisposing or pharmacologic factors?]. 1744 8

Two patients presented with potentially fatal pulmonary oedema after accidental exposure to nitric and hydrofluoric acid fumes during electroplating. Despite aggressive respiratory support, one succumbed to respiratory failure 3.5h after inhalation. The other patient also rapidly progressed to respiratory failure. Extracorporeal life support (ECLS) was started 5h after exposure at the ED. During ECLS, hypoxia improved, but pulmonary oedema shown by chest radiography became aggravated. N-Acetyl cysteine and calcium gluconate were given i.v. on the first day of admission and nebulised for 48 h after exposure. Pulmonary secretions were significantly reduced 24 h after the nebulising therapy began. Ultimately, the patient was discharged without serious pulmonary or neurological complications after 28 days of hospitalisation. In this case, early ECLS, nebulised antioxidant and antidote were available to treat potentially fatal pulmonary oedema after exposure to nitric and hydrofluoric acid fumes.
 ...
PMID:Successful extracorporeal life support after potentially fatal pulmonary oedema caused by inhalation of nitric and hydrofluoric acid fumes. 1750 40

This review describes the ionic heterogeneity manifest in the pulmonary circulation, particularly as it pertains to hypoxic pulmonary vasoconstriction (HPV) and pulmonary arterial hypertension (PAH). Heterogeneity in potassium (K(+)) channels, key regulators of vascular tone, cell proliferation, and apoptosis rates, contribute to the diverse response of vascular segments to hypoxia and to the localization of pathological changes in PAH. Pulmonary artery (PA) and pulmonary vein (PV) smooth muscle cells (SMC) express several K(+) channel families, including calcium-sensitive (KCa), voltage-gated (K(v)), inward rectifier (Kir), and 2-pore channels. Diversity is created by heterogeneous occurrence of alternatively spliced, mRNA species, assembly of heterotetrameric channels from diverse alpha-subunits, and association of channels with regulatory beta-subunits. Local heterogeneity in transcription factor activity may underlie differences in channel expression. Enrichment of resistance PASMCs with O(2)-sensitive K(+) channels, such as K(v)1.5, partially explains the greater HPV in resistance versus conduit PAs. In addition, resistance PAs are unique in having mitochondria which dynamically alter production of reactive O(2) species (ROS) in proportion to PO(2), thereby regulating K(+) channel activity and controlling expression through transcription factors, such as HIF-1alpha. In intraparenchymal PVs, a coaxial layer of cardiomyocytes encompasses a media of typical vascular SMCs. PV cardiomyocytes have rhythmic contraction and their Kir-enriched channels may be relevant to genesis of atrial arrhythmias and pulmonary edema. K(v) channel expression is decreased in PAH, leading to elevations of cytosolic K(+) and Ca(2+) that impair apoptosis and increase proliferation. Understanding ionic diversity may allow development of therapies that locally increase K(+) channel current and expression to treat PHT.
 ...
PMID:Potassium channel diversity in the pulmonary arteries and pulmonary veins: implications for regulation of the pulmonary vasculature in health and during pulmonary hypertension. 1758 56


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