Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

85 cases of cardiac amyloidosis have been collected from the university cardiac departments of France. Four distinct clinical pictures have emerged: 1. Primary cardiac amyloidosis (36 cases) which combines: congestive cardiac failure, ECG signs (extreme axis deviation, low voltage, signs of myocardial necrosis), arrhythmias (67%), and a rapidly fatal outcome (23.2 m +/- 8.5); 2. Cardiac amyloidosis associated with a marked neuromuscular amyloidosis (8 cases), in patients of Portuguese extraction (4 out of 8), with a positive family history (6 out of 8), characterised by arrhythmias (5 out of 8), and with a better prognosis (1 death out of 8); 3. Cardiac amyloidosis associated with a dysglobulinaemia (14 cases) with a clinical picture which is almost identical with that of primary cardiac amuloidosis; 4. Senile cardiac amyloidosis, whose frequency increases with age, may sometimes be discovered at routine post mortem examination, and is characterised by atrial fibrillation (13 out of 27) and its association with anaemia, signs of inflammation, and coronary atheroma.
 ...
PMID:[Cardiac amyloidosis: clinical, x-ray, electric, hemodynamic, developmental and pathological aspects. Apropos of 85 cases collected from French cardiology departments]. 9 54

Postweanling rats maintained on a milk-sugar diet develop a sideropenic anemia, the hemoglobin values falling to less than 30 per cent within 8 to 10 weeks. In that period the heart weight increases by more than 3 times, both ventricles enlarging proportionately. As in other forms of cardiac hypertrophy, a progressive increase in the numbers of connective tissue cells occurs. Ultrastructural and stereologic studies show an appreciable proliferation of the mitochondrial mass in myocardial cells, the mitochondrial fractional volume increasing from a normal of 0.38 to 0.48 per unit cell volume. This quantitative increase is accompanied by a progressive deterioration of the internal cristal structure and the appearance of abnormal, degenerating, and necrotic forms of mitochondria as congestive cardiac failure develops. Myofibrils remain normal. The heart of an anemic rat subjected to an additional workload produced by subdiaphragmatic aortic constriction shows an earlier deterioration of the mitochondrial ultrastructure and stereologic profiles. However, it does not become as large as the heart of the purely anemic animal. In anemic animals with an increased workload, the myofibrillar fractional volume increases from a normal of 0.52 to 0.57 per unit cell volume initially. The active sarcomerogenesis is achieved by Z-band proliferation, which was not observed in the heart of the purely anemic animal. These findings provide a structural basis for the functional and biochemical cardiac deterioration observed in the cardiomegaly induced by chronic anemia.
 ...
PMID:Cardiomegaly in chronic anemia in ratsman experimental study including ultrastructural, histometric, and stereologic observations. 12 72

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
 ...
PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Left ventricular performance was studied in 23 young patients with severe chronic anemia due to beta-thalassemia major and intermedia. The patients were divided into three groups according to the number of blood transfusions they had received. The left ventricle (LV) was enlarged in patients who had not received blood and larger still in patients who had received multiple transfusions. Echocardiography and systolic time interval measurements showed that systolic function of the LV was good in all the patients and that there was no statistical difference in systolic function in patients who had and those who had not received multiple transfusions. Heart rate was increased in the latter group. Stroke index and cardiac index were high, especially in patients in Group 3. The diastolic closure rate (EF slope) of the anterior mitral leaflet and its amplitude of movement were increased, but less so in Group 3; this may reflect an alteration in diastolic LV distensibility. The results indicate that despite the presence of cardiomegaly and severe clinical congestive heart failure, LV performance is well preserved in patients with beta-thalassemia, even in those who have received repeated blood transfusions. Clinical cardiac failure is the consequence of volume overload and abnormal chamber compliance. There was no evidence in this of a congestive cardiomyopathy.
 ...
PMID:Left ventricular function in beta-thalassemia and the effect of multiple transfusions. 16 23

The relation between the heart lesions of thrombotic thrombocytopenic purpura and clinical cardiac dysfunction was studied in 17 autopsied patients. Thirteen of the 17 patients had extensive small-vessel thromboses and in some instances hemorrhages and focal necroses within the heart. Congestive heart failure was present in nine of the 17 patients. Thrombotic microcirculatory cardiac lesions and anemia-related high cardiac output may have contributed to cardiac dysfunction. Serial histologic sections of the cardiac conducting system in 10 patients showed microthrombi in seven and associated hemorrhages in five. Lesions were localized to the atrioventricular node and His bundle parts of the system with sparing of the sinoatrial node and bundle branches. Two patients had electrocardiographic evidence suggesting lesions within conducting tissues. Thrombi and hemorrhages are common findings in the conducting tissues in thrombotic thrombocytopenic purpura and may account for cardiac arrest or transient rhythm disturbances.
 ...
PMID:The heart and cardiac conduction system in thrombotic thrombocytopenic purpura. A clinicopathologic study of 17 autopsied patients. 57 83

A child with homozygous sickle cell disease and transposition of the great vessels had erythrocytosis associated with markedly increased plasma erythropoietin activity. Her clinical course was complicated by neurologic manifestations but not by recurrent sickle cell vasooculsive episodes. The fetal hemoglobin level which had been greater than 25% during the first two years of life gradually decreased to less than 10%. She died at 3 years of age of congestive heart failure and severe anemia. The only sickle cell painful crisis occurred during her terminal illness. It is likely that the high levels of fetal hemorglobin decreased sickling and thus allowed erythrocytosis to develop. Fetal hemoglobin may also have prevented frequent vaso-occlusive events despite the high hematocrit level.
 ...
PMID:Sickle cell anemia and transposition of the great vessels. 62 79

Autoimmune hemolytic anemia often develops in patients with chronic lymphocytic leukemia, particularly elderly women. It is heralded by a drop in the hematocrit, elevation of reticulocytes, development of jaundice, or a rise in the indirect fraction of serum bilirubin. Evidence of hemolysis supports the diagnosis, and a positive result of the Coombs test confirms it. Survival time is considerably shorter in patients who have both diseases than in those with chronic lymphocytic leukemia alone. Presenting symptoms in patients with the two diseases may include weakness, dizziness, fever, or hemorrhagic phenomena. If the anemia is severe, palpitations, otic pulsations, and cardiac decompensation are common. Physical examination may show enlargement of reticuloendothelial structures. On the other hand, some patients may be essentially asymptomatic. The hemolytic process must be treated as a separate entity, as even vigorous treatment of the leukemia often does not control it. Corticosteroid therapy is preferred, with splenectomy as a second line of defense. If the patient is not a good surgical risk, chemotherapy should be considered. Transfusions are usually incompatible but should be risked if progressive congestive failure, neurologic disturbance, angina, or signs of an impending infarct are present.
 ...
PMID:When autoimmune hemolytic anemia complicates chronic lymphocytic leukemia. 63 66

In 214 patients with healed myocardial infarction an assessment was made of the prognostic value of risk factors relating to early postoperative cardiac decompensation which occurred in 50 cases. A significant influence was shown by age (greater than or equal to 75 years), pre-existing heart failure and load insufficiency, hypertension (greater than or equal to 180/95 mm Hg), advanced arteriosclerosis with cerebrovascular and renovascular symptoms, infections with fever or septicemia, emergency operations, lang-lasting surgery, decrease in blood pressure during operations (greater than or equal to 70 mm Hg systolic) and postoperative anemia (less than or equal to 3.5 millions erythrocytes/cmm). The postoperative cardiac failure took a lethal course in 60%. Pathogenetically, the discrepancy between O2-requirement and O2-supply in the previously damaged myocardium is of essential importance during the postoperative stress period.
 ...
PMID:[Risk factors and pathogenesis of postoperative cardiac decompensation (author's transl)]. 81 21

A 17-year-old girl with a clinical diagnosis of adult-type juvenile rheumatoid arthritis developed a severe hepatotoxic reaction to 3.6 g of aspirin per day. This was associated with a microangiopathic anemia and transient congestive cardiac failure. She responded well to steroids, and when all laboratory test findings were back to normal, she was "challenged" with five divided doses of aspirin (total, 3.0 g). This produced a salicylate level of 9.1 g/dl and was associated with an immediate deterioration in liver function test findings and a return of microangiopathic blood features with elevation of fibrin split products and a prolonged prothrombin time. These changes were again reversed by promptly starting steroid therapy. This case suggests that disseminated intravascular coagulation, and its rare association with hepatotoxicity, is a potentially fatal side effect of aspirin therapy.
 ...
PMID:Aspirin hepatotoxicity and disseminated intravascular coagulation. 83 40

25-yr old female identical twins of Italian-American origin concordant for sickle beta-thalassemia were studied to explain their clinical differences. One of them has been severely affected from childhood with one aplastic crisis, an earlier onset of vaso-occlusive crises, and recent cardiac decompensation; the other twin shows no cardiac decompensation. Similar are their degree of anemia, RBC indices, blood volumes, absence of splenic sequestration, depression of pO2, elevation of p50 and 2,3-DPG, hemoglobin composition, and peripheral blood globin-synthetic rates. Regarding differences, the more severely affected has a shorter 51Cr RBC life span, a greater menstrual blood loss, and is more overweight, whereas the less severely affected has functional asplenia by 99mTc scanning and a larger proportion of RBC with decreased cellular deformability. We conclude that in sickle beta-thalassemia: (1) genotype alone does not determine the clinical course; (2) significant differences in clinical course can occur with almost identical hemoglobin composition and globin synthetic rates; (3) cellular deformability changes do not correlate exactly with clinical course; and (4) functional asplenia and leanness may be advantageous.
 ...
PMID:Sickle beta-thalassemia: identical twins differing in severity implicate nongenetic factors influencing course. 98 45


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