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)

A 24-year-old patient was admitted to our hospital because of vertigo, coldness and exercise-dependent pain in the left arm. She reported to have suffered from tuberculosis of the lung and a non-A-non-B hepatitis five years ago. Angiography of the aorta thoracica revealed a complete obstruction of the left arteria (a.) subclavia, stenosis of the a. carotis communis on both sides, of the a. carotis interna and the a. vertebralis on the left side as well as a non-detectable perfusion of the upper and medium segment of the left lung. ESR was elevated with 89/128 mm n.W., a hypochromic anaemia, thrombocytosis, hypalbuminaemia, elevation of alpha 2 and gammaglobulins in serum as well as a reduced quick value were found. AT III and protein C concentrations in plasma were also decreased, whereby protein C activity was reduced additionally. HLA-B-51 was positive. Takayasu's arteriitis was diagnosed by us. High-dose treatment with corticosteroids led to a considerable improvement of the clinical status and laboratory parameters of the patient. As this therapy was not associated with a normalization of protein C and AT III concentrations in plasma, protein C and AT III deficiency could be of significance in the development of Takayasu's arteriitis. Until now protein C and AT III deficiency were not described in patients with Takayasu's arteriitis.
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PMID:[A patient with Takayasu arteritis and protein C and AT III deficiency]. 288 94

Erythropoietin corrects anemia and improves hemostasis, but on the other hand bears a risk of thrombotic complications. Therefore in the present study an attempt has been made to evaluate bleeding time, platelet functions and some hemostatic and fibrinolytic parameters in relation to blood and platelet serotonin before and after 1, 2, 4, 8 and 12 weeks of treatment. 22 chronically hemodialyzed patients were administered with human recombinant erythropoietin (rHuEPO) in a dose of 2000 IU s.c. 3 times a week. Bleeding time was shortened significantly as early as after 1 week of the therapy, whereas hematocrit and hemoglobin increased after 2 weeks. These changes lasted throughout the study. Only a transient rise in platelet count, collagen-induced platelet aggregation, beta-thromboglobulin and VIII:C activity were observed during therapy relative to baseline values. ADP- and arachidonic acid-induced platelet aggregation seemed to be unaffected by rHuEPO treatment, whereas a gradual and progressive enhancement in platelet aggregation in response to ristocetin was found, starting from the 2nd week of the therapy. It lasted throughout the study and correlated inversely with the bleeding time and positively with a rise in both blood and platelet serotonin. rHuEPO did not alter plasminogen, fibrinogen, platelet factor 4, alpha 2 macroglobulin levels, protein C activity and euglobulin clot lysis time. A decline in protein C and S concentrations and antithrombin III activity observed during the therapy were counterbalanced by a fall in the activity of alpha 2 antiplasmin, C1 esterase inhibitor and plasminogen activator inhibitor. It is concluded that rHuEPO may improve platelet/vessel wall interactions possibly by means of serotonergic mechanisms. A lowered activity of inhibitors of fibrinolysis may be regarded as a protection against a general tendency to thrombosis during rHuEPO therapy.
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PMID:A study of platelet functions, some hemostatic and fibrinolytic parameters in relation to serotonin in hemodialyzed patients under erythropoietin therapy. 774 May 5

Recent cohort and case control studies of low-dose combined oral contraceptives (COCs) containing the new generation of progestogens have allowed classification of adverse effects into those which are rare but serious and should be considered risks and those which are more frequent but are less of a threat to health. Low-dose COCs continue to affect coagulation in a complex way, but the risk is less than with the older preparations, and it can be minimized by screening women for a personal or familial history of early or unusual thrombosis and for levels of protein C, S, and antithrombin III. Women with true migraine with focal signs should also avoid using COCs. The relative risk of myocardial infarction (MI) may increase from 4:1 in women with one risk factor (age, smoking, hypertension, hyperlipidemia, and diabetes) to 20:1 with two risk factors and 128:1 with three or more risk factors. In the absence of all risk factors, a recent study indicated that the relative risk of MI with COC use was 1.9 for current and past use. COC use also causes a slight increase in hypertension in most women, especially those who are older or have a family history of hypertension. While the COC can affect carbohydrate and lipid metabolism, the new generation of progestogens has reduced these effects. The COC may accelerate presentation of gallbladder disease in predisposed women. The COC protects against benign breast disease but may increase the risk of breast cancer and cervical cancer slightly. There is a strong link between hepatocellular adenoma and COC use, but the incidence is low. Return to fertility after use has not been a problem. Both estrogenic adverse effects (nausea, dizziness, irritability, weight gain, bloating) and progestogenic adverse effects (vaginal dryness, acne, hirsutism, weight gain, depression, loss of libido) can occur in 50% of women, but these generally disappear after a few months of use. In conclusion, the low-dose, third generation COCs are associated with minimal risks in the absence of other risk factors and have many beneficial effects such as the prevention of ovarian and endometrial cancer; a decrease in pelvic inflammatory disease and ectopic pregnancies; and protection from anemia, primary dysmenorrhea, functional ovarian cysts, and benign breast disease as well as from the morbidity and mortality associated with pregnancy.
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PMID:The combined oral contraceptive. Risks and adverse effects in perspective. 776 40

Twenty chronic hemodialysis patients with renal anemia (hematocrit < 25%) received recombinant human erythropoietin (40 IU/kg body weight 3 x weekly) intravenously after each dialysis. Prior to and at 4, 8 and 12 weeks after commencement of erythropoietin therapy, hematocrit together with hemostasis and microhemolysis parameters were determined. There were significant increases in hematocrit, platelet count and platelet retention, but a significant fall in the initial clearly prolonged bleeding time. Free plasma hemoglobin likewise increased. Conversely, lactate dehydrogenase, prothrombin time, fibrinogen, antithrombin III activity, protein C activity and protein S concentration were all unaltered. The positive effect on bleeding time and platelet retention is most probably caused by an increase in adenosine diphosphate due to the hematocrit-dependent rise in the blood shear stress via physiologic microhemolysis (raised free plasma hemoglobin).
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PMID:Influence of recombinant human erythropoietin on hematological and hemostatic parameters with special reference to microhemolysis. 777 78

Treatment with recombinant human erythropoietin (rhEPO) for the anemia of end-stage renal disease has been associated with thrombotic complications. To detect prothrombotic changes in autologous blood donors given 500 U/kg rhEPO subcutaneously (twice weekly during a 3-week period), changes in variables of hemostasis and fibrinolysis and in blood rheology before and at the end of treatment were investigated. In 21 patients, platelet count increased from 272 +/- 55 x 10(9)/L to 313 +/- 55 x 10(9)/L (p < 0.05). Although activated partial thromboplastin time and protein C antigen decreased significantly during rhEPO treatment, these changes remained within normal ranges. No changes in the hemostatic variables prothrombin time, fibrinogen, factor V, von Willebrand factor antigen, antithrombin III activity, protein S antigen, and prothrombin fragments F 1 + 2 were found. Measurements of plasminogen activity, alpha 2-antiplasmin activity, tissue plasminogen activator, and plasminogen activator inhibitor-1, representing variables of fibrinolysis, were normal and constant during the study. In 5 patients no changes in red cell deformability and whole blood viscosity, corrected for differences in hematocrit, were observed. Plasma viscosity showed a slight but clinically not relevant increase in 4 out of 5 patients. The absence of evident (pro)thrombotc changes in this study confirms the safety of high-dose rhEPO therapy in autologous blood donors, who donate 2 units (i.e., 2 x 450 ml) of blood.
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PMID:The effect of recombinant human erythropoietin on hemostasis, fibrinolysis, and blood rheology in autologous blood donors. 803 97

To clarify the effects of correction of anemia with recombinant human erythropoietin (rHuEPO) on blood coagulation, fibrinolysis and endothelium, these markers were examined in 19 regular hemodialysis patients before and 4, 8, 12 weeks on rHuEPO treatment, and 5 weeks after the end of treatment. Hematocrit significantly increased from 22.8 +/- 2.0 to 31.1 +/- 2.7% at 12 week (p < 0.001). Coagulation and fibrinolysis markers did not show significant changes except for minor and transient alteration of protein C, thrombin-antithrombin III complex and alpha 2-plasmin inhibitor plasmin complex (PIC) throughout the treatment. Endothelin and 6-keto-prostaglandin F1 alpha (PGF1 alpha) significantly increased from 6.1 +/- 4.5 to 14.2 +/- 2.9 pg/ml (p < 0.001) and from 51.9 +/- 14.7 to 66.5 +/- 18.5 pg/ml (p < 0.05) at 12 week, respectively. Human atrial natriuretic peptide (ANP) significantly decreased from 277.9 +/- 88.6 to 179.4 +/- 73.3 pg/ml at 12 week (p < 0.001). Endothelin and PGF1 alpha after 6 month treatment with rHuEPO showed high values as same as those of 12 weeks. These data suggests that rHuEPO therapy did not affect blood coagulation and fibrinolysis, however exerts effects on the endothelium. Changes in endothelial function after rHuEPO may be one of the pathogenetic mechanisms of hypertension and may contribute to a decrease in thrombotic complications.
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PMID:[Changes in endothelial vasoactive substances and blood coagulation and fibrinolysis functions under recombinant human erythropoietin therapy in hemodialysis patients]. 831 81

We studied 37 hemodialysis patients during hemodialysis in order to assess the effects of dialysis on endogenous plasma coagulation inhibitors (antithrombin III, protein C, free and total protein S). The patients were examined prior to erythropoietin (EPO) treatment, upon reaching target hemoglobin (Hb) and after 3 months at steady state Hb levels. The levels of protein C increased significantly during dialysis. However, EPO treatment did not affect the levels of any of the endogenous coagulation inhibitors, either upon reaching target Hb or after 3 months of steady state Hb. The sequence of change during dialysis of protein C, free and total protein S was constant when comparing respective patterns prior to EPO treatment to those at target Hb and steady state Hb respectively. In conclusion, hemodialysis seems to activate synthesis of endogenous coagulation while partial correction of anaemia with EPO does not affect the levels of these inhibitors.
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PMID:Effects of hemodialysis and long-term erythropoietin treatment on protein C, and on free and total protein S. 858 93

Fanconi anemia (FA) is a genetically heterogeneous autosomal recessive syndrome associated with chromosomal instability, hypersensitivity to DNA crosslinking agents, and predisposition to malignancy. The gene for FA complementation group A (FAA) recently has been cloned. The cDNA is predicted to encode a polypeptide of 1,455 amino acids, with no homologies to any known protein that might suggest a function for FAA. We have used single-strand conformational polymorphism analysis to screen genomic DNA from a panel of 97 racially and ethnically diverse FA patients from the International Fanconi Anemia Registry for mutations in the FAA gene. A total of 85 variant bands were detected. Forty-five of the variants are probably benign polymorphisms, of which nine are common and can be used for various applications, including mapping studies for other genes in this region of chromosome 16q. Amplification refractory mutation system assays were developed to simplify their detection. Forty variants are likely to be pathogenic mutations. Seventeen of these are microdeletions/microinsertions associated with short direct repeats or homonucleotide tracts, a type of mutation thought to be generated by a mechanism of slipped-strand mispairing during DNA replication. A screening of 350 FA probands from the International Fanconi Anemia Registry for two of these deletions (1115-1118del and 3788-3790del) revealed that they are carried on about 2% and 5% of the FA alleles, respectively. 3788-3790del appears in a variety of ethnic groups and is found on at least two different haplotypes. We suggest that FAA is hypermutable, and that slipped-strand mispairing, a mutational mechanism recognized as important for the generation of germ-line and somatic mutations in a variety of cancer-related genes, including p53, APC, RB1, WT1, and BRCA1, may be a major mechanism for FAA mutagenesis.
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PMID:Sequence variation in the Fanconi anemia gene FAA. 937 98

Recombinant human erythropoietin (rHu-EPO) in the treatment of renal anemia might predispose to an increased risk of thrombotic complications. In an attempt to comprehend the involvement of the physiologic inhibitors of coagulation in this process, we studied 2 groups of hemodialysis patients. Group I included 21 patients receiving a starting dose of 90 IU/kg/week s.c., and group II included 17 patients without rHu-EPO. The following coagulation tests were performed before rHu-EPO treatment, and after 1, 6 and 12 months: prothrombin time; activated partial fistula thromboplastin time; fibrinogen; plasminogen activity; antithrombin III activity; protein C activity; total and free protein S antigens, and C4b binding protein. Only the latter three parameters were changed in group 1, while high baseline levels of protein S antigens were found in both groups. A decrease in total and free protein S was observed within 1 month of treatment. At the 6th month total protein S returned to near pretreatment values, whereas a significant fall in free protein S (p = 0.007) was observed. All three parameters returned to near baseline values by 12 months. These results suggest that protein S activity can be altered at the beginning of EPO therapy, a change that under favoring circumstances might contribute to the thrombotic events reported during the early phase of rHu-EPO treatment.
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PMID:Effects of long-term treatment with recombinant human erythropoietin on physiologic inhibitors of coagulation. 938 55

Serum hypergastrinemia promotes the growth of colorectal adenocarcinoma. Some colorectal adenomas express cholecystokinin B/gastrin receptor mRNA, and thus hypergastrinemia may increase progression through the adenoma-carcinoma sequence. This was investigated in the multiple intestinal neoplasia APC(Min-/+) mouse. Serum gastrin levels in APC(Min-/+) mice were elevated 5-6-fold by oral administration of omeprazole (75 mg/kg). Terminal tumor burden was monitored by onset of anemia. A labeling index was generated by immunohistochemical detection of bromodeoxyuridine incorporation. Serum gastrin was neutralized by antigastrin antibodies raised in situ by use of a gastrin immunogen, Gastrimmune. Hypergastrinemia resulted in reduced survival of the APC(Min-/+) mice from a median survival of 13 weeks in the controls to 10 weeks following omeprazole treatment (P < 0.00001, log-rank test). The labeling indices of adenomas from the small and large intestines of omeprazole-treated mice were increased 35 and 29%, respectively (P < 0.05 and P < 0.025, respectively). Gastrimmune immunization reversed both the survival effect and the increased proliferation resulting from serum hypergastrinemia. Hypergastrinemia may promote the progression of existing premalignant colonic lesions by increasing proliferation. Clinical investigations should determine whether this occurs in the human scenario, considering the widespread use of proton pump inhibitors.
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PMID:Hypergastrinemia promotes adenoma progression in the APC(Min-/+) mouse model of familial adenomatous polyposis. 1121 60


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