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

Haemostasis has been studied by several authors during exposure to altitude hypoxia. On acute induction to hypoxia, platelet count, platelet aggregability and bleeding time are normal; an increase of thromboxane released from platelets and of prostacyclin, released from endothelial cells is observed; coagulation factors are unchanged except of F. VIII which is increased; modified antithrombin III (ATm) are normal; fibrinopeptide A is increased in subjects with pulmonary edema and fibrinolytic activity after venous occlusion is normal. In chronic hypoxia, during a stay at 6542 m (Mt. Sajama), we found in 7 subjects an important increase in D. Dimer (p < 0.001) that seems to correspond to an activation of coagulation and a decrease of F. VIII R. Cof/F. VIII R. Ag ratio which suggests an endothelial cell damage.
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PMID:Haemostasis at high altitude. 148 90

Reduced oxygen tension is regarded as the primary physiologic signal for the production of erythropoietin (EPO). There is little information available about early changes of EPO production in man due to severe hypoxia. The purpose of the present study was to examine the time course of EPO in serum of patients with acute cardiogenic pulmonary edema (ACPE). In 29 patients (seventy-five +/- six years, mean age +/- SEM) who were hospitalized within two hours after onset of symptoms of ACPE, serum EPO concentrations were monitored for up to seventy-two hours. At the moment of admission all patients showed significantly increased EPO concentrations of 121 +/- 64 mU/mL (mean +/- SEM) compared with a healthy population (15-35 mU/mL). Twenty-three patients who recovered within thirty minutes (group A) exhibited a quick return of their EPO serum levels to normal. The remaining 6 patients (group B) had a protracted clinical course and their EPO concentration showed a further increase up to the end of the observation period. The comparative monitoring of concentrations of alpha-1-proteinase inhibitor, antithrombin III, C-reactive protein, fibronectin, hapotoglobin, and transerrin in serum and plasma revealed no significant changes. Thus a major contribution of fluid shifts into or from the intravascular compartment to the observed changes in EPO concentration seems to be unlikely. The data suggest that the production and release of EPO in the kidneys due to altered oxygen delivery is a fast-responding mechanism.
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PMID:Serum-erythropoietin concentration during acute cardiogenic pulmonary edema. 201 19

The purpose of this study was to investigate the relation between serum lipase (LP), serum immunoreactive trypsin (IRT), and its inhibitors in patients with adult respiratory distress syndrome (ARDS) of diverse origin and to compare their time course with other acute conditions. The IRT and LP levels were determined at regular intervals in 41 patients hospitalized in the intensive respiratory unit with ARDS (n = 9), acute pancreatitis (n = 5), shock (n = 9), bronchopneumonia (n = 10), or acute cardiogenic pulmonary edema (n = 8). Several trypsin inhibitors were measured simultaneously: serum trypsin inhibitory capacity (TIC), alpha 1-antitrypsin, alpha 2-macroglobulin, and antithrombin III. Concomitantly, angiotensin-converting enzyme (ACE) activity was determined as a potential marker of the endothelial injury. A respective 19- and 13-fold increase in IRT and LP values were observed in patients with ARDS after a mean evolution of 6 days; similar increases were seen in patients with pancreatitis. These values were significantly higher than those observed in the other conditions studied. In patients with ARDS and acute pancreatitis, the evolution of IRT and LP values were associated with a sixfold rise in TIC. A low TIC/IRT ratio in patients with ARDS appeared to be an index of poor prognosis. Conversely, ACE activity evolution was characterized by an early decrease in all the conditions studied. These observations indicate that there is an acute delayed pancreas injury in ARDS. Thus, the release of pancreatic enzymes are not reliable markers of the early evolution of the disease but they may represent secondary mediators for enhancement of the increased endothelial permeability.
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PMID:Evidence for pancreas injury in adult respiratory distress syndrome. 298 86

Liver pathology is one of the main features of HELLP syndrome and develops on the basis of a generalised activation of intravascular coagulation. Fibrin deposits and haemorrhagic necrosis predominantly develop in the periportal areas and may eventually lead to subcapsular haematomas or even rupture of the liver. While the compensated form of activation of intravascular coagulation, which is diagnosed by a decrease in antithrombin III and an increase in thrombin-antithrombin III complex (TAT) and the appearance of fibrin, monomers and D-dimers, is found in almost all cases of HELLP syndrome, the decompensated form of intravascular coagulation with prolonged bleeding time (PT, PTT) and drop in fibrinogen is found only in the most severe forms. The development of a decompensation of coagulation correlates with the appearance of severe complications such as liver haematoma, abruptio placentae, renal failure and pulmonary oedema. The best prophylaxis against the development of life-threatening complications is early diagnosis and termination of pregnancy after stabilisation of the maternal condition, consisting of magnesium sulphate infusion, antihypertensive treatment with dihydralazine or calcium antagonists, steroids etc. Severe complications of HELLP syndrome have occasionally been observed in the postpartum period. As prophylaxis against postpartal worsening of HELLP syndrome, curettage of the uterus and continuation of the treatment with calcium antagonists and dexamethasone have been recommended.
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PMID:[Liver pathology within the scope of HELLP syndrome]. 784 9

Neonatal respiratory distress syndrome (RDS) is an acute lung injury believed to result primarily from surfactant deficiency in the immature lung. Although surfactant replacement therapy has improved the outcome of this disease, RDS remains a major cause of neonatal mortality and morbidity. Preliminary experimental evidence suggests that unopposed intravascular thrombin activity may contribute to the progression of RDS by promoting high permeability pulmonary oedema and pulmonary hypertension. In the extravascular lung compartment, polymerizing fibrin may inhibit surfactant function. In addition, interstitial and alveolar thrombin formation and resulting fibrin deposition may contribute to the development of chronic lung disease through amplification of inflammation and fibrosis. There is good evidence that extravascular coagulation occurs during the course of RDS. Fibrin is a major component of the hyaline membranes, which are a hallmark of acute lung injury, and which can be regarded as locally produced clots. It has been less certain whether neonatal RDS is also associated with intravascular activation of the coagulation system. Although low levels of antithrombin III (AT III) have been reported in infants with RDS, direct evidence of increased intravascular thrombin formation has been lacking. However, recently, plasma concentrations of thrombin-antithrombin III (TAT) complexes have been measured in infants with RDS and correlated with RDS severity. TAT formation was significantly increased in severe neonatal RDS, while free AT III activity was decreased. These data are consistent with increased thrombin generation and resulting AT III consumption. Therefore, to regulate thrombin activity, infants with severe RDS may benefit from replacement therapy with AT III concentrate. This hypothesis has been strengthened by experiments that have demonstrated the efficacy of thrombin inhibition in several animal models of acute lung injury. However, controlled clinical trials will be required to determine whether thrombin is just a coincidental marker of neonatal RDS, or whether unopposed thrombin activity exacerbates the disease process.
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PMID:Antithrombin III deficiency in neonatal respiratory distress syndrome. 818 52

A 24-year-old woman was infected with falciparum malaria during travel to Kenya, complicated by intravascular coagulation and pulmonary edema. She was successfully treated with anti-malarial drugs including chloroquine, quinine sulfate and pyrimethamine, with a combined regimen of heparin, antithrombin III and nafamostat mesilate for disseminated intravascular coagulation, and with methylprednisolone pulse therapy for pulmonary edema. The present case emphasizes the importance of early diagnosis and appropriate treatment in terms of falciparum malaria. This case, in particular, is believed to be worth reporting as overseas travel is increasing and yet anti-malarial drugs are not readily available to most physicians in Japan.
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PMID:Falciparum malaria in an overseas traveler complicated by disseminated intravascular coagulation and pulmonary edema. 840 May 1

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.
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PMID:A pheochromocytoma causing limited coagulopathy with hemoptysis. 1595 97

For an extended period of time various research projects have been conducted on the relationship of hypoxia and haemostasis. The enclosed article contains the conclusion to which extent lack of oxygen can activate the coagulation system and induce a prothrombotic state. The majority of studies proved a shortening of coagulation times during acute exposure to hypoxia, whereas activated parameters of coagulation and fibrinolysis like prothrombin fragment F1+2 as well as thrombin-antithrombin III complexes and D-dimer remained mostly unmodified. It is suggested that a prolonged sojourn at high altitudes could lead to activation of the coagulation system through an increase of haematocrit and blood viscosity. Recently it was proven that people living at high altitudes show an enhanced risk of stroke incidents. The significance of the change in haemostasis on that outcome has not yet been part of the research. However, it has been proven that the activity of the coagulation system does not play a pathophysiological part in the development of acute mountain sickness and high altitude pulmonary edema. Recent studies also demonstrated that moderate hypoxia during long haul flights may not be the main trigger in inducing deep vein thrombosis in passengers.
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PMID:[Interaction of hypoxia and haemostasis--hypoxia as a prothrombotic factor at high altitude?]. 1596 61

In this study, we report a 15-year-old female with end-stage renal disease undergoing hemodialysis, who admitted with acute respiratory failure and generalized edema. Abdominal tomography detected thrombi in the right renal vein, in the hepatic segment of the inferior vena cava and in iliac veins. Levels of proteins C and S, antinuclear antigen, anti-dsDNA, C3, and C4 were in normal limits. The thrombi persisted despite treatment with nadroparin, heparin with fresh frozen plasma and warfarin. Due to heparin resistance, antithrombin III levels were measured and were found abnormally low. The first echocardiographic examination was in normal limits but the second echocardiography revealed a huge thrombus occluding the tricuspid valve. Urgent thrombectomy was planned but the patient died in the intensive care unit due to severe pulmonary edema.
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PMID:A huge intracardiac thrombus developed in the presence of antithrombin III deficiency in a patient with end-stage renal failure. 2416 98