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)

In pediatric cardiology tcPO2 is useful in monitoring cyanotic children given high-risk therapy such as balloon septostomy or drugs with controversial effects such as tolazoline in persistent fetal circulation. tcPO2 during administration of 100% oxygen enables a rapid, noninvasive differentiation between cyanosis due to intracardiac right-to-left shunt and that due to low cardiac output or pulmonary ventilation or diffusion difficulty. The size of the right-to-left shunt can be roughly estimated from the highest value of tcPO2, this estimation being influenced by anemia, hypothermia, and acidosis, among other factors. A trend of the tcPO2 rise is evident 90 seconds after the beginning of oxygen breathing. If tcPO2 does not rise at least 40 mm Hg over the initial value, a significant right-to-left shunt must be suspected. Interpretation of tcPO2 rise is difficult in dynamic right-to-left shunt, changing with oxygen breathing.
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PMID:tcPO2 in pediatric cardiology: application during balloon septostomy, tolazoline administration, and in children with right-to-left shunt. 53 16

The clinical aspects of Hemoglobinopathy S in children of a black family from Zair living in Belgrade are discussed in the paper. The parents and two brothers are heterozygous carriers for patologyc hemoglobines; those children had, sauf permanent anaemia, the crysis of dyspnea, cyanosis, cough, evidence of subperiosteal bone formation, associated with vitamin D deficiency. The Youngest child, girl two years of age, is homozygous with complete Sickle cell disease: hand-foot syndrome, heterotopic paravertebral hematopoetic tissue, lung infarctions, cardiomegaly, severe drepanocytic anaemia; she succumbed in an a attack after many episodes of severe hypoxia.
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PMID:[Hemoglobinpathy S--clinical manifestations in children in a Zairian family]. 61 14

Acute acetaminophen intoxication was studied in the dog to characterize pathogenesis and in the mouse as a model for antidotal research. In the dog, overt toxicity was manifested principally by cyanosis, facial and paw edema, gastrointestinal disturbance, and coma. Typical laboratory findings were methemoglobinemia, hemoconcentration, leukocytosis, and hepatic centrolobular necrosis. In the mouse, physical signs of acetaminophen overdose appeared to be central in origin; sequelae included anemia, leukopenia, thrombocytopenia, and hepatic centrolobular necrosis. The antidotal profile of acetylcysteine in mice was characterized. When acetylcysteine therapy was instituted early (one hour after acetaminophen overdose), it conferred dose-related protection from lethality coupled with hepatoprotection, as judged from transaminase activity. When acetylcysteine therapy was instituted relatively late (4 1/2 hours after acetaminophen overdose), its beneficial effect on survival persisted but was unaccompanied by distinct hepatoprotection, indicating that SGPT activity was an unreliable prognostic indicator. Acetylcysteine was well tolerated in mice even when administered in the presence of preexisting acetaminophen-induced liver damage.
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PMID:Pathophysiology of acetaminophen overdosage toxicity: implications for management. 72 40

A screening survey for abnormal hemoglobins at a hospital in Mizunami city, Gifu prefecture, Japan detected a fast-moving variant of hemoglobin in a family of Japanese origin. The abnormal hemoglobin constitutes about 45 percent of the total hemoglobin from the propositus and another carrier in the family, but neither of these persons had anemia, jaundice, cyanosis or splenomegaly. Structural analysis of this hemoglobin revealed that the amino acid substitution was at residue 83 in the beta chain, where a glycine was replaced by an aspartic acid. This hemoglobin variant has been previously reported in a Greek child (hemoglobin Pyrgos) (1). Oxygen affinity of hemoglobin Pyrgos was found to be normal.
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PMID:Hemoglobin Pyrgos (beta83 Gly replaced by Asp) in a Japanese family. 89 27

Administration by the owner of three 325-mg (5-gr) tablets of acetaminophen (N-acetyl-p-aminophenol) to each of 2 adult Burmese cats was associated with severe illness of both cats and death of one. Administration of two 325-mg tablets to each of 2 experimental adult cats resulted in severe illness. Marked cyanosis was observed in experimental cats within 4 hours after administration of one 325-mg tablet. Cyanosis was apparently due to anoxia associated with conversion of hemoglobin to methemoglobin by acetaminophen or its metabolites. Anemia, hemoglobinuria, and icterus were subsequently observed in the cats. Anemia and hemoglobinuria were caused by intravascular hemolysis of red blood cells (RBC). Icterus was due to both lysis of RBC and hepatic necrosis. Facial edema developed in 3 of 4 cats, but the pathogenesis of this lesion was not determined. The doses of acetaminophen were extremely large; however, administration of comparable doses to cats by their owners is a potential hazard because the drug is available without prescription as a 325-mg tablet. From information available at present, it seems that acetaminophen administration to the cat causes more dramatic clinical signs and is more likely to be fatal than the same doses of salicylates. Because phenacetin is metabolized to acetaminophen, similar clinical signs may occur in cats given phenacetin.
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PMID:Acetaminophen toxicosis in the cat. 111 50

Human red blood cells (RBCs) are subject to an enormous degree of genetic diversity. The variability that occurs may result in anemia, cyanosis, polycythemia, or may cause no hematologic alterations. Genetic abnormalities affecting hemoglobin include the sickling disorders, the unstable hemoglobinopathies, hemoglobinopathies associated with polycythemia or with methemoglobinemia, and the alpha- and beta-thalassemias. The most common enzymatic abnormality of RBCs is glucose-6-phosphate dehydrogenase deficiency, but defects of many other enzymes leading to hemolytic anemia have been identified. Deficiences of RBC enzymes may also be important in the diagnosis of nonhematologic disease and in the evaluation of dietary status.
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PMID:Genetic disorders of human red blood cells. 117 73

Haemoglobin M is a rare cause of congenital cyanosis and is usually misdiagnosed as being due to congenital heart disease. This was also the case in a family on whom this report is based. In five members of three generations the characteristic grey-blue cyanosis was due to a haemoglobin M anomaly. In all of them cardiopulmonary disease, anaemia and haemolysis had been excluded. The amino-acid substitution was in the alpha-chain of the globin molecule. Consequently the carriers of the trait have an abnormal haemoglobin content of 20-25%. Despite marked cyanosis they feel well.
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PMID:[Haemoglobin M-Homburg (author's transl)]. 125 2

We found that an abnormal hemoglobin with a very low oxygen affinity was responsible for overt cyanosis in an otherwise healthy adolescent. Hemoglobin Beth Israel, in which serine replaces the asparagine residue normally present at position 102 (G4) of the beta-polypeptide chain, was associated with normal blood counts and no apparent exercise intolerance in the heterozygous carrier. Cyanosis resulted from a drastically right-shifted oxygen dissociation curve, whose position and shape could account for the absence of "physiologic" anemia. The whole-blood oxygen tension at 50 per cent oxygen saturation was 88 mm Hg (normally 26 +/- 1 mm Hg), and the arterial blood was only 63 per cent saturated with oxygen despite a normal oxygen tension of 97 mm Hg. The hemolysate showed a low oxygen affinity but normal Bohr effect. Unexplained cyanosis, particularly in association with normal arterial oxygen tension should prompt a search for an abnormal hemoglobin, which may obviate the need for invasive diagnostic procedures.
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PMID:Hemoglobin Beth Israel. A mutant causing clinically apparent cyanosis. 127 28

Treatment of choriocarcinoma is mostly successful but there is still appreciable mortality from early respiratory failure. A series of 135 patients with choriocarcinoma presenting with dyspnea between 1960 and 1988 was studied to find prognostic factors for early respiratory death and to identify how mortality may be further reduced. Mortality with respect to early respiratory death (ERD) was 11% and was significantly associated with WHO prognostic score, chest X-ray appearance, central cyanosis, tachycardia, anemia, and clinical evidence of pulmonary hypertension. Indicators on chest X ray of high risk of ERD were the presence of more than 10 opacities, extensive opacification of lung fields, size of metastases, and hazy background obscuring the vascular pattern. Intensity of initial treatment was not correlated with this outcome. A set of criteria has been derived which will predict ERD with 100% sensitivity and 38% positive predictive value. These are opacification of lung fields on chest X ray of more than 50%, OR initial plasma hCG level greater than 10(5) when there is anemia and a history of chest pain. Patients presenting with choriocarcinoma and dyspnea who fulfill these criteria should be considered for extracorporeal perfusion techniques. As respiratory failure in this condition is characterized by hypoxemia and right-to-left shunting, extracorporeal perfusion should be effective. Ventilation should be avoided as no patient survived mechanical ventilation.
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PMID:Respiratory failure due to choriocarcinoma: a study of 103 dyspneic patients. 169 17

Three physicians selected ten basic physical findings for a study of diagnostic decision making in the global assessment of patients. The physicians independently examined 201 hospital in-patients for the presence of each of the findings and concluded their assessment with a global evaluation of whether the patient appeared ill. Each of the ten findings were used by at least one of the physicians in his overall assessment of the patient. All the observers considered 'looking older than age', 'trouble with breathing', 'cyanosis', and 'anaemia' important, but disagreed in their use of the remaining findings (P less than 0.01). Agreement in the global clinical assessment is an essential prerequisite to uniformity in the approach to the patient.
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PMID:Global assessment of patients--a bedside study. I: The influence of physical findings on the global assessment. 276 77


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