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)

An haematological, biological, parasitological and immunological study about anaemia of pregnancy was carried out in two rural village of Mali Republic, where P. flaciparum malaria is hyper-endemic. The 25 pregnant women found in the villages were compared with 23 controls. One could observe that anaemia more often normochromic and regenerative usually appears during the second trimestre of pregnancy. Only a few cases with haemaglobin levels below 8 g. % are hypochromic. Serum transferrin levels were slightly higher among pregnant. None among 31 bone marrows examined showed megaloblastic changes. Haptoglobin levels below 10 mg. % were observed in 3/4 of the pregnant women versus 1/4 in controls. Like some others, this study confirms the primary responsability of malaria haemolysis in the aetiology of anaemia of pregnancy and the interest of systematic chemoprophylaxis, at least from the third month of pregnancy. Vitamin and iron therapy is to consider therafter in hyper-endemic areas of P. falciparum malaria when nutritional problems are not predominant.
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PMID:Malaria and anemia of pregnancy in an African savanna zone. Epidemiological, hematological, biological and immunological study of 2 villages of the Bamako region, Republic of Mali. 58 Sep 10

Plasma concentrations of the acute phase proteins (APP), C-reactive protein (CRP) and haptoglobin (Hp), increased markedly following experimental infection of dogs with Trypanosoma brucei. The highest concentrations of CRP were observed immediately after peaks of parasitaemia. Treatment with curative doses of the trypanocidal drug suramin caused a rapid decrease in CRP. Relapse infections after subcurative treatment were followed by a reappearance of high plasma CRP concentrations. Haptoglobin remained elevated during the course of the disease. Curative treatment with suramin caused a gradual but slow decrease in Hp while subcurative treatment caused no significant changes. Thus, the estimation of CRP was useful in determining the presence of active infection and the success of chemotherapy. High Hp levels in severely anaemic dogs indicated that intravascular haemolysis does not contribute significantly to the anaemia associated with T. brucei infections in dogs. These conclusions need confirmation from a larger experiment.
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PMID:Elevation of the concentration of acute phase proteins in dogs infected with Trypanosoma brucei. 168 Feb 82

A 60-year-old man was admitted to our hospital because of fever, hemorrhagic tendency, anemia and neurological abnormality. A blood count revealed that the hemoglobin was 6.8 g/dl, the reticulocyte was 17.3 percent with 2 erythroblasts per 100 white cells, the white cell count was 7,100/microliters and the platelet count was 0.8 x 10(4)/microliters. Peripheral blood smear demonstrated marked fragmentation of red cells. Bone marrow examination disclosed the marked erythroid hyperplasia. Although the bleeding time was prolonged (14 minutes 30 seconds), the other hemostatic data were within normal limits. The serum bilirubin level was 1.57 mg/dl; LDH level, 1,437 U/l; creatinine level, 0.92 mg/dl; BUN level 14.7 mg/dl. Haptoglobin was below 10 mg/dl. Results of immunological tests were all negative except the result of PAIgG (576.6 ng/10(7) cells). The urinalysis showed proteinuria, microhematuria and trace granular and hyaline casts. A diagnosis of thrombotic thrombocytopenic purpura was made. The patient was initially treated with prednisolone (60 mg), aspirin (1,000 mg), dipyridamole (150 mg), gabexate mesilate (1.5 g), sodium oxagrel (80 mg) daily with little response. The thirty days after admission, infusion of gamma globulin (20 g, daily) was given for 3 days. The clinical state and laboratory findings became dramatically improved shortly after the administration of gamma globulin and the laboratory data came to be normalized after 1 month. After ten months of this treatment, the patient is remained asymptomatic and the hematological data are within normal range without using any drug. A trial seems justified to confirm the value of this mode of therapy.
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PMID:[Thrombotic thrombocytopenic pupura (TTP)--remission following treatment with high-dose immunoglobulin]. 177 57

Hemophiliacs often have mild anemia, and hemolysis has been suggested as the likely mechanism on the basis of the reduced serum haptoglobin values frequently observed in these patients. It has been suggested that hypohaptoglobinemia results from isohemagglutinins or other contaminating proteins in the infused factor concentrates. The advent and increased utilization of Factor VIII concentrates that are highly purified by use of monoclonal antibodies have provided the opportunity to study whether proteins other than Factor VIII contained in the concentrate induce hemolysis. Of 49 consecutively studied Factor VIII-deficient hemophiliacs, 19 (39%) had a reduced serum haptoglobin level (less than 27 mg/dl). In particular, 16 of 35 (46%) of patients receiving only monoclonally purified Factor VIII products (Monoclate or Hemofil-M) had a reduced serum haptoglobin value. Haptoglobin measurements were variable on repeat measurement in 8 patients. Haptoglobin levels did not correlate with type or severity of hemophilia, hemoglobin value, or alterations in liver function. Low serum haptoglobin values were also observed in children with leukemia, without apparent hemolysis, who had extensive cutaneous hemorrhage associated with thrombocytopenia. We propose that reduced serum haptoglobin values in hemophiliacs do not result from immune-mediated hemolysis due to contaminating proteins in the concentrate. Moreover, hypohaptoglobinemia may not be due to hemolysis at all but may instead result from dissolution of hematomas and other foci of internal hemorrhage.
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PMID:Reduced serum haptoglobin values in hemophiliacs receiving monoclonally purified factor VIII concentrates. 210 38

Haptoglobin (Hp) polymorphism and its relationship to malaria infections was examined in Solomon Islanders under 25 years of age. The slide positive rate for malaria was 48% (53/111): Plasmodium vivax (Pv) 21 cases, Plasmodium falciparum (Pf) 16 cases and the remaining 16 were a mixture of Pv/Pf/P. malariae. Of 111 subjects examined, 17% (19 subjects) were ahaptoglobinemic (HpO). No association was observed between HpO and parasitemia, gender, anemia, serum insulin-like growth factor-1 (IGF-1) level, blood glucose level and enlargement of the spleen. These results suggest that malaria may not be the major cause of HpO in the people of the Solomon Islands.
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PMID:Relationship of haptoglobin polymorphism to malaria in the Solomon Islands. 764 99

Immunosuppression of recipients of renal transplants with azathioprine has been associated with two major side effects: hepatotoxicity and myelotoxicity, mainly in the form of leukopenia. Reports of isolated anemia in these patients have been rare. We now observed the development of severe anemia in 9 out of 11 renal transplant recipients whose immunosuppressive regimen was converted from cyclosporine plus prednisone to azathioprine plus prednisone. A significant (P = 0.001) drop in hematocrit (from 34 +/- 4% to 27 +/- 3%, mean +/- SD) and hemoglobin (from 11.6 +/- 1.3 g/dl to 9.5 +/- 1.0 g/dl) was found. Since a common variable of all these patients was their use of an angiotensin-converting enzyme (ACE) inhibitor as antihypertensive medication, we speculated that the combination of azathioprine and ACE blocker might be the reason for the anemia. We then compared 2 groups of 10 patients each who had been on azathioprine as their regular immunosuppressive agent and who did or did not take an ACE inhibitor. Hematocrit and hemoglobin were significantly (P = 0.01) lower in the group of patients taking ACE inhibitors (33 +/- 6% versus 41 +/- 5% and 11.5 +/- 2.0 g/dl versus 14.0 +/- 1.6 g/dl, respectively). Haptoglobin levels were also significantly (P = 0.05) lower in the ACE inhibitor group (116 +/- 65 mg/dl versus 210 +/- 114 mg/dl). Erythropoietin concentration in the serum and the reticulocyte index were slightly, but not significantly, higher in the ACE inhibitor group but the values were probably too low for their degree of anemia. Comparing hematological parameters of the patients in the ACE inhibitor group before and after beginning of the antihypertensive treatment confirmed a significant reduction of hematocrit and hemoglobin following therapy with an ACE inhibitor. Hematocrit fell from 41 +/- 7% to 36 +/- 6% and hemoglobin from 14.0 +/- 2.3 g/dl to 11.3 +/- 1.5 g/dl (P < 0.05 for both). We conclude that the combination of these two drugs should probably be avoided.
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PMID:Anemia in renal transplant recipients caused by concomitant therapy with azathioprine and angiotensin-converting enzyme inhibitors. 821 54

About 220 children (110 boys and 110 girls) aged 18 months to 10 years, 65.9% have been selected from anamnesis, clinical, and biological criteria to produce reference values on specific proteins dependent inflammatory, anemia and hemolysis (C-reactive protein = CRP; Transferrin = TRF and Haptoglobin: HPT). Specimens have been analysed by Nephelometric immuno-chemical method. For the two groups, A1 [18 months-5 years] and A2 [5-10 years], the reference values of the whole study population are reported: CRP (A1 3.35 +/- 3 mg/l: A2 2.40 +/- 2.30 g/l, with a significant difference at Student Fisher "t" test p < 0.03); TRF (A1 4.05 +/- 1.5 g/l; A2 4.50 +/- 1.4 g/l; NS, p > 0.05) HPT (A1 2.55 +/- 2.0 g/l: A2 1.20 +/- 1.10 g/l; S(r) p < 10(-5)). Furthermore, for TRF, HPT we must consider the sex in the results meaning because of significant difference into boys and girls.
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PMID:[Selection criteria for the establishment of reference values in tropical zones. Application to specific proteins: C-reactive protein, haptoglobin, transferrin in gabonese children]. 926 48

Haptoglobin phenotypes have been shown in human medicine to be related to the prevalence of various diseases. Furthermore, abnormal glycosylation of haptoglobin has been reported as a consequence of liver disease, cancer and immunological disorders in man. To our knowledge, similar findings have not, so far, been reported in canine disease. The present paper describes a method for investigation of canine haptoglobin phenotypes and of microheterogeneity caused by altered glycosylation. The method consisted of isoelectric focusing (IEF) of dog serum, followed by immunoblotting. The results indicated the existence of only one canine haptoglobin phenotype with a characteristic microheterogeneity pattern in healthy dogs. Changes in this pattern were found in serum from dogs with liver disease, predominantly chronic progressive hepatitis, and with different kinds of anaemia. Pretreatment of serum with neuraminidase or glycopeptidase F (PNGase F) resulted in identical IEF patterns of haptoglobin from healthy and diseased dogs. Moreover, a fucose-specific lectin was capable of binding to some of the abnormal haptoglobin fractions, mainly those found in association with anaemia. The changes described were interpreted as alterations of the carbohydrate content, with or without fucosylation, of some haptoglobin fractions.
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PMID:Disease-related variations of the glycosylation of haptoglobin in the dog. 980 25

Mitomycin C is a powerful antineoplastic agent. If used at high dosage, it may cause a secondary form of adult hemolytic-uremic syndrome (HUS). Blood transfusions worsen the evolution of this peculiar form of HUS. We describe a patient who developed HUS after treatment with mitomycin C (total dose 144 mg/m2) due to a carcinoma of the ascending colon. Repeated blood transfusions were associated with rapidly evolving renal failure coupled with anemia and thrombocytopenia. Haptoglobin was undetectable. Soon after starting subcutaneous erythropoietin, the velocity of progression of renal failure slowed whilst no more blood transfusions were required and haptoglobin levels returned to normal. Thereafter, the patient's renal function slowly worsened and she started chronic hemodialysis 5 years later. Up to now, all investigations have failed to show a relapse of her adenocarcinoma. A possible explanation of these data is that erythropoietin permitted the termination of blood transfusions which both triggered and perpetuated the syndrome. However, we cannot exclude a primitive effect of erythropoietin on the endothelium or on the platelets.
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PMID:Erythropoietin is beneficial in mitomycin-induced hemolytic-uremic syndrome. 1205 72

Severe malarial anaemia (SA) is a major complication of malaria and an important cause of child mortality and morbidity. However, the pathogenesis behind SA is poorly understood. Nitric oxide (NO) is known to play a protective role against clinical malaria but is also suggested to have a pathogenic role in cerebral malaria (CM). Erythrophagocytosis by splenic macrophages has been implicated in the pathogenesis of SA. In this study, plasma levels of NO, neopterin, haptoglobin and C-reactive protein (CRP) were measured in paediatric patients with CM, n=77, SA (n=28) and uncomplicated malaria (UM n=53). Haptoglobin levels were significantly lower in SA (median (interquartile range) 25 (17-59) mg/l) than in both CM and UM (40 (24-80) mg/l and 110 (60-160) mg/l, respectively, P<0.001). In contrast, NO levels were higher in SA (38 (28-51) micromol/l) than in CM and UM (21 (15-32) micromol/l and 10.3 (5.6-17) micromol/l, respectively, P<0.001). A significant negative correlation between haptoglobin and NO was seen in the SA group. No such correlation was observed within the UM or CM groups. No significant differences in neopterin levels were observed between any of the three groups, neither was there any correlation between parasitaemias and neopterin levels. The low haptoglobin and high levels of NO in this SA group may contribute to haemolysis. Taken together our results support the hypothesis that immune-mediated erythrocyte destruction is involved in the pathogenesis of malarial anaemia.
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PMID:Elevated levels of nitric oxide and low levels of haptoglobin are associated with severe malarial anaemia in African children. 1208 54


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