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)

The aims of this study were to determine the presence of Babesia spp. in blood samples from Italian dogs with clinical signs compatible with tick-borne diseases by means of PCR-restriction fragment length polymorphism (RFLP) and describe the clinicopathological findings of dogs with Babesia infection. We evaluated the majority of canine babesiosis cases by means of clinical history, physical examination, hematological, biochemical, serum electrophoresis, urinalysis and hemostatic tests. Forty-five out of 164 canine blood samples studied were positive to Babesia PCR-RFLP with the following results: Babesia canis canis (n=34) and Babesia canis vogeli (n=11). The majority of B. c. canis infections were detected in Northern Italy (29.1%; 30/103). B. c. vogeli cases were detected mainly in Central and Southern Italy (16.3%; 10/61). Only one B. c. vogeli was detected in Northern Italy (0.9%; 1/103). Three positive samples to B. c. canis and four positive samples to B. c. vogeli were selected for sequencing of a fragment of the 18S rRNA gene (410bp) for further molecular characterization. The sequence obtained from all seven dogs was 99/100% homologous to sequences from B. c. canis and B. c. vogeli, respectively, present in GenBank. Sixty-two percent of dogs infected with B. c. canis had recently travelled on a hunting trip to East European countries. The main acute clinical signs were dehydration, apathy, anorexia and fever. The majority of dogs infected with B. c. canis presented at initial clinical examination mild to severe thrombocytopenia, hyperfibrinogenemia, mild to moderate normocytic-normochromic non-regenerative anemia, hemolysis and neutropenia. The urinalysis showed hemoglobinuria in 13/19 dogs suggesting intravascular hemolysis. Dogs with B. c. canis infection had high levels of C-reactive protein. Hypoalbuminemia was present in 17/26 dogs. The 11 cases of B. c. vogeli infection did not present a homogenous clinicopathological pattern. B. c. vogeli infections were observed in young dogs causing hemolytic anemia and in adult/old does that frequently presented predisposing factors such as splenectomy or immunocompromised conditions. In conclusion, this study demonstrates the presence of B. c. canis and B. c. vogeli in Italian sick dogs and differences in clinicopathological pattern in these two species of B. canis.
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PMID:Babesia canis canis and Babesia canis vogeli clinicopathological findings and DNA detection by means of PCR-RFLP in blood from Italian dogs suspected of tick-borne disease. 1878 81

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired hemolytic anemia caused by somatic mutations in the phosphatidylinositol glycan-complementation class A gene and the resulting absence of a key complement regulatory protein, CD59. Affected red blood cells in patients with PNH undergo intravascular complement-mediated lysis with resulting anemia, hemoglobinuria, and venous thromboses. Hepatic venous outflow thrombosis [Budd-Chiari syndrome (BCS)] is especially common in PNH patients and often fatal. The few case reports of outcomes in patients undergoing liver transplant for BCS secondary to PNH detail instances of recurrent BCS as well as early thrombotic portal vein occlusion and hepatic artery thrombosis requiring retransplantation. PNH is therefore generally considered a contraindication to liver transplantation. Here we present the first report of a patient with PNH and BCS undergoing successful liver transplantation while receiving eculizumab, a humanized monoclonal antibody that blocks the activation of the terminal complement at C5.
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PMID:Successful liver transplantation for Budd-Chiari syndrome in a patient with paroxysmal nocturnal hemoglobinuria treated with the anti-complement antibody eculizumab. 1939 43

Four pasture-fed Japanese Black cows showed the main clinical symptoms of severe hemoglobinuria at different periods between 2003 and 2007. Hematological analyses at the first consultation revealed severe anemia, and biochemical analyses indicated both severe hemolysis and disruption of hepatic function. Although the first 2 patients died, the hemoglobinuria and general condition of the remaining 2 cows, who were immediately initiated on large doses of antibiotics, improved within 3 days. Clostridium haemolyticum was detected by polymerase chain reaction (PCR) analysis of the blood sample of 1 of the infected cows. Anti-fascioliasis medicine is administered, and since then, no case of hemoglobinuria has been observed. The cows were diagnosed with bacillary hemoglobinuria, and they represent the first few cases in Japan.
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PMID:Successful treatment of bacillary hemoglobinuria in Japanese Black cows. 1972 68

Occurrence of the rare CD16b deficiency ("null" phenotype) in neutrophils from two female patients (41 and 15 years old) is reported. The first case was referred with a diagnosis of anemia related to paroxistic nocturnal hemoglobinuria and the second case, with presumptive diagnosis of immune neutropenia. In both cases, absence of CD16b expression was determined by flow cytometry without deficiencies of other neutrophil alloantigens or defects of membrane anchorage through glycosil phosphatydil inositol (GPI) linkage. Clinical manifestations in both patients could not be attributed exclusively to the absence of CD16b, as other receptors for the IgG Fc fragment (CD32 and CD64) could compensate this deficiency that occurs in <1% of the caucasic population. Nevertheless, it is important to take this rare deficiency into account in order to prevent isoantibody formation after eventual blood transfusions, or transient neonatal immune neutropenia in children born to women with the "null" phenotype.
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PMID:[Neutrophils without CD16b receptors]. 1977 99

The development of RBC autoantibodies resulting from or associated with allogeneic blood transfusions is not an easily determined complication of RBC transfusions. This report discusses one patient who developed RBC autoantibodies in association with an allogeneic blood transfusion and alloimmunization leading to a temporary bystander immune hemolysis. A 72-year-old woman was hospitalized as a result of severe anemia and received two units of ABO- and D-compatible RBCs. She had a history of two pregnancies 40 years before, but no history of RBC transfusion, and her antibody screen was negative. On the tenth day after transfusion her hemoglobin dropped, and alloanti-c was identified in her serum and eluate. At this time she received another two units of compatible blood according to her phenotype (group O, R1R1, K:-1). After 48 hours, she developed joint pain, pyrexia, and hemoglobinuria, and her Hb dropped from 9.2 g/dL to 5.3 g/ dL. The direct antiglobulin test was positive, an IgG autoantibody was present in the eluate, and the antibody investigation revealed the presence of anti-Jk(b) in addition to the previously identified alloanti-c. Her genotype was determined, and, based on the findings, two additional units were selected, found to be compatible, and transfused without incident. Transfusions were discontinued, and she was treated with IVIG and corticosteroids. Her Hb increased to 9.7 g/dL, and the patient made an uneventful recovery. It was concluded that transfusion of incompatible RBCs induced the formation of an autoantibody in this patient, resulting in lysis of bystander RBCs. The need for additional blood transfusion was successfully avoided by treatment with IVIG, steroid therapy, and rituximab.
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PMID:Autoantibody formation after alloimmunization inducing bystander immune hemolysis. 1985 26

Blood destruction due to a single injury, as by sodium oleate, or acting through a short period of time, as by toluylenediamine or hemolytic immune serum, is not characterized, in the absence of hemoglobinuria, by an increased elimination of iron in the urine. This holds, not only for the evanescent injury caused by sodium oleate, but also for the severe type caused by hemolytic immune serum, in which a progressive destruction of the blood may persist for 2 weeks or more with constant evidence of the disintegration of erythrocytes as shown by bile pigment in the urine. This finding is in accord with previous investigations of anemia in both man and animals. Likewise, no striking increase is evident, under such circumstances, in the percentage of iron excreted in the feces. The total amount of iron in the feces has been notably increased in two experiments with hemolytic serum, but as the percentage was not appreciably altered, the difference depends presumably on variations in the bulk of feces rather than upon increased elimination. This evidence of the power of the body to conserve the iron rephagocytosis is negligible, is to be fragmented one by one, while still circulating, to a fine, hemoglobin-containing dust. The cell fragments are rapidly removed from the blood, but their ultimate fate remains to be determined. The facts indicate that they are removed from the blood by the spleen, and under exceptional conditions, by the bone marrow.
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PMID:THE ELIMINATION OF IRON AND ITS DISTRIBUTION IN THE LIVER AND SPLEEN IN EXPERIMENTAL ANEMIA. 1986 17

In rabbits transfused almost daily with the whole citrated blood of other rabbits, an extraordinary condition often develops, which manifests itself in an almost immediate clumping together of all the red cells in specimens of the shed blood. This clumping is due to one or more true agglutinins, of which the strength may be such as to cause clumping in a 1: 2,800 plasma dilution. The agglutinating principle circulates with the corpuscles against which it is effective; but under ordinary circumstances intravascular clumping fails to occur because the union of antigen and antibody can take place only at a temperature several degrees below that of the body. If the temperature is sufficiently lowered, as when a tourniquet is applied to the rabbit's ear, intravascular clumping ensues. In defibrinated blood, gradually cooled, clumping is first noted as the temperature of 35 degrees C. is approached; and at room temperature (22 degrees ) the corpuscles will often come together in a short time into a single, solid mass. At 0 degrees C. the agglutination is still more marked. The reaction seems to be completely reversible, for when the blood is warmed again, the clumps break up and disappear at between 35 degrees and 36 degrees C. Cooling and warming with the resultant clumping and dissociation can be carried out many times on the same blood specimen without apparent change in the corpuscles or in the rapidity of the reaction. The response to temperature changes is extremely prompt. Once it has been elicited, the agglutinating principle may persist for a long time after the transfusions are stopped, in one instance it was still strong 133 days after the last transfusion. During this period the plethora was succeeded by a severe anemia, which in turn was recovered from. In many rabbits no agglutinin develops, and a continuance of the transfusions will not elicit it. Indeed, when present it tends to disappear if the transfusions are persisted in. In several of the animals in which the agglutinin was strongest, the plethora was suddenly succeeded by severe anemia, despite continued transfusions. The character of the temperature control of the agglutination, which somewhat resembles that of the hemolysin in paroxysmal hemoglobinuria, has led us to consider whether the blood destruction might not be due to accidental chilling of the animal. Efforts to induce a fall in the hemoglobin by placing the rabbit's ear in ice water have as yet been unsuccessful. Thus far no adequate search for an hemolysin has been made. The object of the present paper has been to describe a condition in which large amounts of free antigen and antibody circulate together in the organism, and to demonstrate the factor which prevents their union, the results of which could easily be fatal. The causes of the condition will be dealt with in a subsequent communication.
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PMID:FREE ANTIGEN AND ANTIBODY CIRCULATING TOGETHER IN LARGE AMOUNTS (HEMAGGLUTININ AND AGGLUTINOGEN IN THE BLOOD OF TRANSFUSED RABBITS). 1986 23

1. A method is described whereby toxic substances may be extracted from hemolytic streptococci with inactivated serum. 2. Such extracts contain large amounts of hemotoxin and leucocidin. 3. Their intravenous injection into mice causes marked hemoglobinuria, anemia, and death. 4. There is evidence that this anemia is not the only cause of death of these animals. 5. Incomplete work seems to indicate that the hemotoxin and the lethal poisons are not antigenic. 6. Certain biological properties of the extract are described.
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PMID:THE TOXIC PROPERTIES OF SERUM EXTRACTS OF HEMOLYTIC STREPTOCOCCI. 1987 Feb 33

A 7-year-old female Boston terrier was referred to Hokkaido University Veterinary Teaching Hospital with a history of hemoglobinuria and anemia for several days. Abdominal radiographs showed splenomegaly, and ultrasonography revealed a hypoechoic splenic parenchyma with interspersed linear echoes consistent with the ultrasonographic appearance of splenic torsion. Ultrasonography and computed tomography (CT) indicated a C-shaped spleen. Exploratory laparotomy confirmed the diagnosis of splenic torsion. A splenectomy was performed, and the dog recovered well without complications. This is the first report of splenic torsion in Boston terriers, and the usefulness of ultrasonographic and CT findings of the splenic torsion was also confirmed.
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PMID:Primary splenic torsion in a Boston terrier. 1995 8

Anemia affects many active patients, from young female recreational athletes to elite male competitors. The treatment may simply be iron supplementation, but the causes of iron-deficiency anemia are many, including poor nutrition, exercise-induced hemoglobinuria or hematuria, gastritis, hemorrhoids, peptic ulcer disease, angiodysplasia, and adenocarcinoma. Therefore, physicians need to do a thorough evaluation that includes a medical history, family medical history, drug history, physical exam, and referral to a gastroenterologist if necessary.
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PMID:Evaluating and treating active patients for anemia. 2008 22


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