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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major causes of anaemia in pregnancy in tropical Africa are malaria, iron deficiency, folate deficiency and haemoglobinopathies: now there is added also the acquired immune deficiency syndrome (AIDS). Anaemia is often multifactorial, with the different causes interacting in a vicious cycle of depressed immunity, infection and malnutrition. Anaemia progresses through 3 stages: compensation, with breathlessness on exertion only; decompensation, with breathlessness at rest and haemoglobin (Hb) below about 70 g/litre; cardiac failure, with Hb below about 40 g/litre. Without treatment, over half of the women with haematocrit less than 0.13 and heart failure die. Maternal anaemia, malaria and deficiencies of iron and folate cause intrauterine growth retardation, premature delivery and, when severe, perinatal mortality. Surviving infants have low birthweights, immune deficiency and poor reserves of iron and folate. They have entered already the vicious cycle of infection, malnutrition and impaired immunity. Treatment with blood transfusions is even more hazardous since the advent of AIDS, and should be limited to saving the life of the mother. Treatment of malaria is complex as chloroquine-resistant strains are now common. Prevention remains relatively easy with proguanil and supplements of iron and folic acid and is highly cost-effective in the improvement of maternal and infant health; it is more important than ever as it avoids the unnecessary exposure of women and infants to HIV transmitted through blood transfusion.
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PMID:Tropical obstetrics and gynaecology. 1. Anaemia in pregnancy in tropical Africa. 269 76

Iron chelation therapy must be associated with the regular blood transfusions required for thalassaemia and other chronic anemias. We report here a study concerning 4 groups of patients, aged 6 to 28, regularly transfused at Necker Enfants-Malades hospital: a) 20 with thalassaemia major; b) 6 with thalassaemia intermedia; c) 2 with sickle cell disease and d) 2 with Blackfan-Diamond syndrome. The transfusion regimen consisting of monthly or quarterly transfusions varied as a function of the groups. Desferal was used in all patients. The dosage and the route of administration (IV, IM, SC) were adapted to the amount of iron transfused and to the nature of the disease. The serum ferritin level was considered as the indicator of the iron overload. Comparisons were established between the quantities of iron transfused, ferritin levels, and parameters such as dosage, route of administration and compliance to Desferal. During the period of study 3 patients died from cardiac failure due to transfusional hemosiderosis. Endocrine complications (diabetes 2 cases, hypocalcemia 3 cases, hypothyroidism 1 case and delayed puberty 7 cases) were observed. This high incidence of complications induced by post-transfusional iron overload has recently prompted us to improve the quality of chelation therapy through the use of the services of a specialized center where patients as well as their families can be trained more adequately in home care and self-treatment.
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PMID:[Treatment of post-transfusion iron overload by deferoxamine]. 273 4

Iron, iron-binding capacity, lactoferrin and total protein were determined in the plasma and pleural fluid of 30 patients with cardiac failure (n = 10), infectious/inflammatory disease (n = 9) and metastatic carcinoma (n = 11). In 16 patients pleural transferrin and ferritin was also measured. Plasma iron and total iron-binding capacity were reduced in inflammatory and neoplastic disease, whereas hyposideremia with normal iron-binding capacity was seen in patients with heart failure. Plasma lactoferrin was reduced in metastatic carcinoma. Exudates (protein greater than or equal to 30 g/l; infectious/inflammatory: 9/9, carcinomatous: 10/11) had significantly higher iron, lactoferrin, transferrin and ferritin concentrations than transudates (protein less than 30 g/l; heart failure: 10/10, carcinomatous: 1/11). Statistically, infectious/inflammatory exudates could be distinguished from neoplastic exudates by a higher median iron concentration (non-parametric Wilcoxon-Mann-Whitney test). Overlap of the respective ranges, however, did not allow a clear-cut differential diagnosis in individual cases. Pleural lactoferrin concentrations, on the other hand, correlated with the pleural granulocyte count and nonspecifically reflect the degree of granulocytic inflammation. Positive pleural/plasma correlations of protein and of iron concentrations were found in exudates only. Within exudates and transudates, on the other hand, total protein correlated with transferrin but not with iron concentrations. Therefore, and because of the substantially higher pleural/plasma ratio for iron than for transferrin concentrations, a quantitatively important, non-transferrin bound iron pool in pleural fluids, most probably ferritin, must be assumed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Iron and iron-binding proteins in the differential diagnosis of pleural effusion]. 276 88

Idiopathic hemochromatosis is a hereditary disease characterized by a progressive iron overload secondary to high intestinal iron absorption. After a latent period of many years, manifestations of liver cirrhosis, diabetes mellitus, cardiac failure, hypogonadism, skin hyperpigmentation and arthropathy can occur. Liver cirrhosis is the most common feature and it is complicated by hepatocellular carcinoma in 30% of cases. Tests of high sensibility are available for early diagnosis. Repeated phlebotomy can prevent clinical features in asymptomatic patients and can improve prognosis in symptomatic subjects. Current concepts in idiopathic hemochromatosis are reported in this review.
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PMID:[Idiopathic hemochromatosis]. 298 52

Hereditary hemochromatosis is the most common cause of iron overload in adults and is probably the second most common cause of iron overload in children in the United States next to transfusional overload. Serious morbidity from this disorder of iron absorption can occur in early as well as in middle and advanced age, iron overload having been reported in children with hereditary hemochromatosis as early as 2 years of age. Younger persons differ from older persons in that the risk for iron loading in females appears to be equal to the risk for males, in contrast to a preponderance of males among older patients. Also, younger patients frequently demonstrate cardiac and gonadal involvement, with cardiac failure commonly leading to death, whereas older patients are more likely to have liver involvement and diabetes mellitus, with liver failure and hepatoma commonly leading to death. Because early diagnosis and treatment can prevent the toxicities of iron overload, appropriate screening can be lifesaving. Transferrin saturation is the most reliable screening test. Liver biopsy with objective measurement of hepatic iron stores is the most important diagnostic criterion at present, although reliable noninvasive methods for quantitating body iron are being developed. Young individuals who should be screened for iron overload include patients with cardiac myopathies, hypogonadism, amenorrhea, loss of libido, diabetes mellitus, other endocrine disorders, cirrhosis of the liver, and arthritis, as well as the siblings, parents, and children of patients with hereditary hemochromatosis or iron loading of unknown cause.
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PMID:Hereditary hemochromatosis in children, adolescents, and young adults. 305 60

Pathologic findings in six beta-thal major, 58 beta-thal Hb E, and 12 Hb H patients were presented. The causes of death were mainly infection in the first and second decades and cardiac failure in older patients. There was accelerated intramedullary and extramedullary erythropoiesis, with a few cases showing focal fibrosis, some with decreased cellularity and occasional atypia. Iron deposition mirrored that of thal patients in the European and American literature, apart from minimal cardiac siderosis, and the correlation between the amount of iron deposited and dysfunction of the particular organ was not always apparent. Patients with Hb H disease showed a less extensive iron deposition and organ pathology than those with the other two types of thalassemia.
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PMID:Pathologic findings in 76 autopsy cases of thalassemia. 339 May 38

Ferritin (F) is an iron-protein (molecular weight 445.000) present in various organs including the heart. Using the immunoenzymatic method (Ferrizyme Abbott), ferritinemia (Fe) was determined daily in 28 patients with acute myocardial infarction (AMI). A significant rise was revealed, already evident in the first few days 8-9 after with Fe gradually returns to baseline levels. The results have shown that this pattern is not evident in patients with angina, heart failure, valve defects, pericarditis or cor pulmonale and may thus be considered a reliable, if not early, marker of myocardial cytolysis. In those cases studied no correlations were observed between CPK and Fe peak or between these and clinical intensity of AMI.
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PMID:[Behavior of blood ferritin in acute myocardial infarct]. 355 38

A case of intoxication with 5 g of elemental iron (25 g of ferrous sulfate) in a 30-year old woman at 36 weeks gestation is reported. Deferoxamine treatment was given with a delay of 26 hours after ingestion. A healthy infant was delivered by cesarean section 31 hours following ingestion. Subsequently, the patient developed hepatic necrosis, coma and hemostatic dysfunction and expired in cardiac failure after two weeks. The fatal outcome supports the view that the potential lethal dose of iron is lower for adults than for children. This case also demonstrates that major hepatic dysfunction can be a prominent feature of adult cases of iron intoxication. It is not unequivocal that early institution of deferoxamine treatment would have had a significant influence on the outcome. However, taking into account the well-documented efficacy of the drug in children and that no major adverse fetal effects have been associated with deferoxamine treatment in pregnancy, we suggest such antidote therapy to be considered for prompt institution in similar cases.
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PMID:Fatal iron intoxication in late pregnancy. 366 20

Peroxidation of lipids was studied in patients with heart failure after coronary heart disease and acquired valvular diseases. Even at early stages of the heart failure an increase in the concentration of dien conjugates, malonic dialdehyde and intensification of the peroxidation of blood lipids under stimulation by bivalent iron have been revealed. These changes do not depend on reasons which caused heart failure.
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PMID:[Lipid peroxidation in cardiac insufficiency]. 377 89

In idiopathic hemochromatosis, there is progressive deposition of iron in parenchymatous organs owing to a defect in iron absorption the nature of which is not so far known. This can result in cardiomyopathy with heart failure and arrhythmia which are refractory to therapy. Nuclear magnetic resonance tomography is a specific imaging technique for early detection of myocardial iron deposits. With quantitative determination of the T2 relaxation time of the myocardium, a progress control under venesection therapy is possible above and beyond diagnostics.
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PMID:[Cardiomyopathy in idiopathic hemochromatosis. Diagnostic possibilities using proton spin tomography]. 382 47


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