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

Dinitrotoluenes (DNTs) are nitroaromatic compounds appearing as pale yellow crystalline solids at room temperature. Dinitrotoluenes exist as a mixture of 2 to 6 isomers, with 2,4-DNT, and 2,6-DNT being the most significant. About 500 persons are estimated to be potentially exposed yearly to 2,4-DNT and 2,6-DNT during the production of munitions and explosives. The main route of human exposure at ammunition facilities is inhalation, but dermal contact and inadvertent ingestion can also be substantial. In factory workers, exposure to DNTs has been linked to many adverse health effects, including cyanosis, vertigo, headache, metallic taste, dyspnea, weakness and lassitude, loss of appetite, nausea, and vomiting. Other symptoms including pain or parasthesia in extremities, abdominal discomfort, tremors, paralysis, chest pain, and unconsciousness have also been reported. The primary targets of DNT toxicity are the hematopoietic system (pallor, cyanosis, anemia, and leukocytosis), the cardiovascular system (ischemic heart disease), the nervous system (muscular weakness, headache, dizziness, nausea, insomnia, and tingling pains in the extremities) and the reproductive system (reduction of sperm counts, alteration of sperm morphology, and aspermatogenesis). An association between DNT exposure and increased risk of hepatocellular carcinomas and subcutaneous tumors in rats, as well as renal tumors in mice, has been established. Epidemiologic studies of DNT toxicity have been limited to small groups of workers who had been occupationally exposed at various ammunitions production facilities. Clearly defining the health effects of DNTs with a high degree of confidence has therefore been difficult because of the multigenic nature of occupational exposure. In an attempt to update the toxicologic profile of the DNTs, we hereby provide a critical review of the environmental and toxicologic pathology of DNTs, with a special emphasis on their potential implications for public health.
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PMID:Environmental toxicology and health effects associated with dinitrotoluene exposure. 1467 15

In this study, thirty male Wistar rats/group were exposed nose-only to mean analytical concentrations of 9.2, 32.4, 96.5, and 274.9 mg aniline/m3 using an exposure regimen of 6 h/day, 5 days/week for 2 weeks (days 0-11), followed by a 2-week post-exposure period (up to day 28). Serial sacrifices for specialized examinations were performed on days 0, 4, 11, 14, and 28. Clinical signs of toxicity, body weights, hematology, and clinical chemistry tests, including total iron in liver and spleen, splenic lipid peroxidation, organ weights, gross and histological changes in target organs were recorded. No mortality was observed during the study. Rats exposed to 96.5 mg/m3 and above displayed cyanosis, with no apparent progression during the exposure period. The predominant manifestation of toxicity was methemoglobin formation and associated erythrocytotoxicity. The changes observed included anemia, red blood cell morphological alterations (e.g., Heinz bodies), decreased hemoglobin and hematocrit, reticulocytosis, and effects on the spleen (splenomegaly, hemosiderin accumulation, and increased hematopoietic cell proliferation), which gained significance at 96.5 and 274.9 mg/m3. With regard to increased splenic extramedullary hematopoiesis, borderline effects occurred at 32.4 mg/m3. The total content of iron in spleen homogenates increased in a concentration-dependent and time-dependent manner with increasing duration of exposure. The maximum accumulation of iron in the liver and spleen exceeded the respective control levels by approximately 60% and approximately 500%, respectively. Splenic lipid peroxidation and total iron were highly correlated (r2 = 0.93) toward the end of the exposure period. A hepatic hemosiderosis was observed at 274.9 mg/m3. Thus, in regard to erythrocytotoxicity and associated increased splenic sequestration of erythrocytes, iron accumulation and lipid peroxidation 32.4 mg/m3 constitutes the no-observed-adverse-effect concentration (NOAEC). However, spleens of the 32.4 mg/m3 exposure group exhibited a minimal increase in extramedullary hematopoiesis. Exposure to 9.2 mg/m3 was not associated with any significant effect.
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PMID:Subacute inhalation toxicity of aniline in rats: analysis of time-dependence and concentration-dependence of hematotoxic and splenic effects. 1518 35

An 18-year-old woman without previously documented medical history delivered a healthy 32-week-old preterm infant. Severe bleeding occurred during week 1 postpartum secondary to ruptured vaginal condylomas. The consequent anemia was accompanied by complaints of exercise intolerance that resolved with blood transfusion. Six weeks later, the patient was brought to the emergency department of the regional medical center, where she was found to be unresponsive, with a left-sided hemiparesis and with hypoxemia that failed to correct with assisted ventilation and 100% oxygen. A cardiology consultation was obtained, which identified the patient as having central cyanosis and heretofore unappreciated marked clubbing of fingers and toes. This suggested a diagnosis of right-to-left shunting, likely at the cardiac level, together with presumptive embolic stroke, which was documented by magnetic resonance imaging and magnetic resonance angiography as a left pontine infarct. Transthoracic and transesophageal echocardiography identified anomalous drainage of the inferior vena cava into the left atrium, which was confirmed by a three-dimensional computed tomographic angiogram. Corrective surgery in the form of atrial septostomy and redirection of the inferior vena cava to the right atrium was performed. The patient was subsequently discharged and is in stable condition 3 months later without effort intolerance and with normal arterial oxygen saturation on room air.
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PMID:Central cyanosis and clubbing in an 18-year-old postpartum woman presenting with a stroke. 1576 23

We retrospectively reviewed 34 consecutive patients with serologically confirmed leptospirosis admitted during years 1992-2002. Nine patients (26.5%) had respiratory symptoms on admission including cough (n = 4), shortness of breath (n = 4), cyanosis (n = 2), and hemoptysis (n = 1). Six patients had pulmonary radiographic findings including (1) diffuse, ill-defined, ground-glass density (n = 3); (2) diffuse alveolar opacities (n = 2); and (3) small nodular density (n = 1). Male/female ratio was 8/1 and mean age was 47 years. Seven patients reported their exposure source including hunting (n = 2), fishing (n = 2), fresh water swimming (n = 2), and canoeing (n = 1). All patients had fever (mean = 40.1 degrees C). Other common symptoms were headache (n = 4), vomiting (n = 3), and myalgia (n = 3). Biological abnormalities included elevated liver enzymes (n = 8), proteinuria (n = 7), lymphopenia (n = 6), hematuria (n = 5), renal failure (n = 4), anemia (n = 4), and elevated neutrophil count (n = 4). PaO(2 )was measured for 3 patients while they were breathing room air (32, 55, and 66 mmHg). Suspected diagnosis on admission included leptospirosis (n = 2), bacterial pneumonia (n = 2), intoxication, influenza, viral hepatitis, biliary tract lithiasis, and rapidly progressive glomerulonephritis (one patient each). The first serologic testing for leptospirosis was positive for 5 patients (55%). Serovar was presumptively identified for 7 patients: Australis (n = 3), Grippotyphosa (n = 2), and Icterohaemorrhagiae (n = 2). Seven patients were treated with penicillin; two patients received no antibiotics. All patients were cured. In conclusion, patients with leptospirosis may present predominantly with nonspecific pulmonary symptoms. In these patients, leptospirosis must be suspected when there is a potential exposure to rats, especially in case of high-grade fever, myalgia, hepatitis, and renal abnormalities.
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PMID:Respiratory manifestations of leptospirosis: a retrospective study. 1621 64

The erythropoietic system plays a major role in tissue oxygenation because the erythrocytes are the primary carriers of oxygen in the form of oxyhemoglobin. Therefore, clinical entities such as abnormal hemoglobins, polycythemia, anemia, and significant changes in blood volume frequently produce alterations in various respiratory functions. The pulmonary manifestations can vary from mild respiratory illness to life-threatening emergencies with high mortality rates. Among the hemoglobinopathies, sickle cell disease is clinically the most important and commonly associated with serious pulmonary consequences, including acute chest syndrome, pneumonia, infarction due to in situ thrombosis, bone marrow fat embolism of pulmonary vasculature, bone marrow infarction, pulmonary hypertension, and other abnormalities. Hemoglobinopathies with high and low affinity for oxygen and other abnormal hemoglobinopathies occasionally cause clinically significant respiratory complications by interfering with normal tissue oxygenation. Acquired methemoglobinemia can cause alarming cyanosis and medical emergency. Erythrocyte disorders are associated with pulmonary complications, including pulmonary hypertension, alveolar fibrosis, and pulmonary dysfunction. Coagulation disorders, both the inherited and acquired types, have the potential to affect the respiratory system in the form of hemorrhage from the airways, lung parenchyma, or pulmonary hypertension. The following paragraphs describe the common pulmonary complications and manifestations associated with hemoglobinopathies, erythrocyte disorders, and coagulation abnormalities.
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PMID:Lungs in hemoglobinopathies, erythrocyte disorders, and hemorrhagic diatheses. 1626 4

Haemoglobinopathies constitute entities that are generated by either an abnormal haemoglobin or thalassaemias. While abnormal haemoglobins are caused by a qualitative structural abnormality of the haemoglobin molecule, thalassaemias result by diminished synthesis of the globin chain. Due to increased immigration from Asia, Africa and the Mediterranean to Northern Europe, haemoglobin S, haemoglobin C, haemoglobin E are also encountered commonly in Switzerland, while other abnormal haemoglobins are rare, yet can cause clinically relevant symptoms. This include haemolysis, polyglobulia, cyanosis or a combination thereof Thalassaemia-syndroms constitute with two million affected individuals to the most prelevant monogenetic diseases worldwide. Due to migration into Switzerland, they are also found quite commonly among our patients with 10-15 per cent of all hypochromic, microcytic, anemia second only to iron deficiency. Importantly, thalassaemias and haemoglobinopathies can occur concomitantly sometimes even with a normal haemoglobin variant. This results in wide-spread presentations, making diagnosis and clinical judgement difficult. We describe in this article not only physiological mechanisms and clinical presentation but also propose a step-wise diagnostic algorithm including selective use of molecular biology methods.
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PMID:[Hemoglobinopathies--clinical symptoms and diagnosis of thalassemia and abnormal hemoglobins]. 1645 Jul 33

The Norwood procedure with a modified Blalock-Taussig shunt (MBTS) is the first of the three-stage surgical palliation for infants with hypoplastic left heart syndrome. We report a patient with schistocytic hemolytic anemia that developed following a right MBTS with a Gore-Tex graft. Hemolysis associated with a MBTS has not been previously reported in the literature. Multiple packed red blood cell transfusions were required due to desaturation and hypoxemia. Hemi-Fontan procedure was performed early for chronic anemia. Hemolysis resolved post operatively even though the patient subsequently required a Gore-Tex central shunt for persistent cyanosis.
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PMID:Hemolytic anemia secondary to modified blalock-taussig shunt. 1743 50

Placental malaria is recognized as a common complication of malaria in pregnancy in areas of stable transmission, and, as a consequence, serious health problems arise for the mother and especially her baby [1]. Although malaria in pregnancy is a major factor associated with adverse perinatal outcome, the link between malaria and perinatal morbidity/mortality is less clear in areas with stable endemic malaria where pregnant women have acquired immunity [2]. Histological examination of the placenta is a predictor of fetal morbidity, as well as being the most sensitive detector of maternal infection [3]. Adverse perinatal outcome has been described as an important indicator of poor quality of obstetric care and social development [4]. A variety of adverse perinatal outcomes associated with placental malaria have been described, including low birth weight, preterm delivery, intrauterine growth retardation, fetal anemia, congenital malaria, and fetal mortality. The most common clinical features in 80 percent of perinatal cases are fever, anemia, and splenomegaly [5]. Other signs and symptoms include hepatomegaly, jaundice, regurgitation, loose stools, poor feeding, and, occasionally, drowsiness, restlessness, and cyanosis also can be seen [5,6].A review of studies that investigated these poor fetal outcomes associated with placental malaria in sub-Saharan Africa is presented here.
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PMID:Impact of placental Plasmodium falciparum malaria on pregnancy and perinatal outcome in sub-Saharan Africa: II: effects of placental malaria on perinatal outcome; malaria and HIV. 1829 21

These data prove that abnormally high oxygen unsaturation of the blood is a cause of cyanosis. The fact that the lowest value of oxygen unsaturation (in the venous blood) associated with cyanosis is about 8 volumes per cent seems to indicate that this amount of reduced hemoglobin is the lowest capable of producing a cyanotic color. We shall later discuss this point more in detail. Table III shows furthermore that in spite of the fact that cyanosis is due to abnormally high oxygen unsaturation, no proportionality exists between the intensity of the blue color and the amount of reduced hemoglobin. This may in small part be due to individual peculiarities of the skin and subcutaneous tissue, which are known to influence in anemia the relation between paleness of the skin and the decrease in hemoglobin. We shall, however, in the succeeding paper show that the main cause of the disproportionality between cyanosis and venous oxygen unsaturation is found in another factor, the recognition of which throws a clearer light on the pathogenesis of cyanosis, and explains why we may find values of oxygen unsaturation as high as 13 volumes per cent in non-cyanotic individuals.
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PMID:STUDIES ON CYANOSIS : I. PRIMARY CAUSES OF CYANOSIS. 1986 57

Idiopathic pulmonary hemosiderosis (IPH) is a rare disorder (triad of iron-deficiency anemia, hemoptysis, and alveolar infiltrates). A 3-year-old male presented with mild fever, breathlessness, dry cough, and bluish nail discoloration for 8 days. He had required five blood transfusions in the past 1 year (last transfusion was given 4 months ago). He had a respiratory rate of 58/min with respiratory distress, cyanosis, and grade III clubbing. Respiratory system examination was normal. Several previous reports of hemoglobin were as low as 3.6 g/dl with hypochromic and microcytic anemia. There were transient increases in the hemoglobin and normalization of red cell morphology with blood transfusions. Serum iron, G6PD enzyme assay, hemoglobin electrophoresis, the sickling test, Coomb's test, stool and urine analysis, and a Meckel's scan were normal. HIV antibody and dsDNA were negative. The chest radiograph revealed symmetrical patchy infiltrates sparing lung apices (confirmed on high-resolution computed tomography). Lung biopsy diagnosed pulmonary hemosiderosis (interstitial lung disease with hemosiderin-laden macrophages scattered in the alveoli and areas of fibrosis in the alveolar septa). The patient showed marked clinical improvement in 10 days of therapy with prednisolone. IPH should be listed in the differential diagnosis of a child presenting with unexplained hypochromic, microcytic anemia and respiratory symptoms.
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PMID:Idiopathic pulmonary hemosiderosis: alveoli are an answer to anemia. 2120 22


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