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)

Epidermolysis bullosa dystrophica is a rare disease that affects the skin and mucous membranes. Manifest at birth, it is characterized by poor dentition, esophageal strictures, syndactyly, and severe chronic anemia. Our 12-year-old patient required extensive dental treatment which necessitated overcoming problems of anesthesia as well as developing a technique of management that provided maximum safety and a minimum of discomfort. Transmission electron microscopy of sections of the gingiva revealed possible degenerative collagen fibers and an interrupted basement membrance. Anchoring fibrils normally found in the connective tissue beneath the epithelium were absent.
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PMID:Epidermolysis bullosa dystrophica polydysplastica. A case of anesthetic management in oral surgery. 26 79

Platelet functions and blood coagulation have been regularly investigated in 31 patients undergoing maintenance haemodialysis for 5 months to 6 years. Fifteen of them suffered from at least two arteriovenous fistula thrombosis during the year prior the first examination. Eleven patients, including eight with recurrent thrombosis, received 300-400 mg per day dipyridamole during 1 month to 2 years. Some abnormalities are commonly observed in the whole studied population: lowering of platelet adhesiveness, defective aggregation in the presence of both collagen and ADP 5. 10-5 M; increased level of factor V and mainly factor VIII. Mean platelet factor 3 activity was in the normal range with variations from one case to another. The only unusual feature observed in patients with recurrent thrombosis was an increase of platelet aggregation induced by ADP 0.5. 10-6 M. Neither spontaneous aggregation nor significant abnormality of plasminogen level and plasma antithrombin activity were observed. Under dipyridamole therapy, correction of platelet hyperaggregability was observed in all patients and improvement of platelet adhesiveness in half the studied cases (despite the unchanged anaemia). The treatment significantly decreased the frequency of arteriovnous fistule thrombosis in the six patients observed during two consecutive years, the first one without and the second under treatment: the total number of thrombosis was 18 during the first and 3 in the second period.
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PMID:[Disorders of haemostasis in patients undergoing maintenance haemodialysis, with special reference to recurrent arteriovenous fistula thrombosis. Effects of dipyridamole (author's transl)]. 82 31

Pentamidine isethionate is a trypanocidal drug used for the treatment of Pneumocystis carinii pneumonitis. Hematological complications have occasionally been reported and include anemia, leukopenia, and thrombocytopenia. We report here several qualitative abnormalities of in vitro platelet function and coagulation that have not been described previously. Platelets were exposed in vitro to concentrations of pentamidine isethionate ranging from 0.5 to 100 mug/ml of platelet-rich plasma. Clot retraction, platelet adhesiveness to glass beads, and platelet aggregation (adenosine 5'-diphosphate [ADP], thrombin, epinephrine, collagen, and ristocetin) were inhibited in a dose-dependent fashion. The addition of pentamidine isethionate after aggregation had been initiated with ADP reversed both primary and, to a lesser degree, secondary aggregation. Platelet factor 3 availability and serotonin uptake and release (using collagen as the releasing agent) were not inhibited. Serotonin release with 10(-4) M ADP was slightly inhibited. Pentamidine isethionate prolonged the thrombin time of plasma at concentrations of 5 mug/ml and greater. The prothrombin time was prolonged at concentrations greater than 10 mug/ml of plasma. The inhibition of aggregation was reversed by washing and resuspension in plasma or by the addition of calcium or magnesium ions.
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PMID:In vitro inhibition of platelet function and coagulation by pentamidine isethionate. 92 Dec 38

Collagenous and microscopic colitis have been described as causes for abundant watery diarrhea with a normal radiologic and endoscopic aspect of the colonic mucosa. Microscopic colitis is characterized by diffuse intraepithelial lymphocytic infiltration and collagenous colitis by thickening of subepithelial collagen layer greater than 15 microns with or without inflammatory changes of the mucosa. Here are reported 5 patients with microscopic colitis and 4 with collagenous colitis. The mean age was 52 years (range 40 to 68) with an equal sex distribution. Diarrhea was of longstanding duration without weight loss, anemia or hypoalbuminemia. Occasionally the volume of diarrhea was over 1 L a day. One patient had steatorrhea that proved resistant to a gluten free diet. Endoscopic and radiologic findings were normal in every patient and the diagnosis was based on typical histology. Azulfidine therapy was successful in 7 patients and prednisone in another. Colonic biopsy should be performed in every patient with chronic diarrhea.
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PMID:[Microscopic colitis and collagenous colitis. An entity not yet reported in Chile]. 134 Sep 62

The effect of dialyzer geometry, both flat plate (FP) and hollow fiber (HF), on platelet and granulocyte activation during dialysis with cuprophane membranes was studied in 12 patients. A subset of six patients was restudied after correction of their anemia with recombinant human erythropoietin (EPO). Granulocyte count and aggregation in vitro fell significantly (P less than 0.01) at 20 minutes of dialysis, followed by a gradual return towards pre-dialysis values at 240 minutes. Malondialdehyde (MDA), a product of free radical reactions generated by activated granulocytes, increased significantly during dialysis [predialysis MDA (median, range): 8.4 (5.8 to 11.6) nmol/ml, 240 minutes MDA: 9.7 (6.6 to 12.5) nmol/ml, P less than 0.01 Wilcoxon test). This increase, however, was not affected by dialyzer geometry or EPO therapy. Neither type of dialyzer was associated with significant platelet loss at the end of dialysis. Whole blood platelet aggregation in vitro (spontaneous and collagen-induced) decreased significantly, (P less than 0.01) during dialysis, the fall in spontaneous aggregation being significantly less following EPO therapy [spontaneous aggregation 240 minutes; pre-EPO: 34 (13 to 52)%; post-EPO 50: (16 to 76)%, P less than 0.01)]. The ratio of the platelet release proteins beta-thromboglobulin and platelet factor 4 increased significantly during dialysis, indicating platelet activation in vivo, although there was no effect of dialyzer geometry or EPO. Factor VIII von Willebrand Factor antigen, a putative marker of endothelial damage, was raised pre-dialysis, and increased further during dialysis, irrespective of dialyzer geometry or EPO. In conclusion, dialyzer geometry had no significant effect on granulocyte and platelet counts and activity during hemodialysis with cuprophane membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dialyzer geometry during hemodialysis with cuprophane membranes. 140 28

In a retrospective study of 352 patients with primary myelodysplastic syndromes, 61 (17.3%) revealed myelofibrosis in bone marrow biopsies. The fibrosis was observed to occur mostly focally (41/61 cases), and collagen deposits were found very rarely (4/61). The histopathology of bone marrow biopsies revealed hyperplasia and disturbed differentiation in megakaryopoiesis; the frequency and grade of dysplasia in megakaryopoiesis increased with advancing myelofibrosis. Reticulin fibrosis occurred in all subtypes of MDS; however, there was a higher incidence in chronic myelo-monocytic leukaemia (CMMoL). The frequency of cytogenetic aberrations was significantly higher in the MDS cases with myelofibrosis, compared to the cases without fibrosis. Clinical data showed significantly lower values of haemoglobin and lower platelet counts in MDS with myelofibrosis. Life expectancy was reduced to 9.6 months, compared with 17.4 months in MDS without fibrosis. In refractory anaemia, the survival times were 10.0 months in MDS with myelofibrosis, compared to 28.9 months in MDS without myelofibrosis. 36.6% of the patients with MDS and myelofibrosis developed a transformation into ANLL during the course of the disease. Myelofibrosis therefore seems to herald a poor prognosis.
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PMID:Myelofibrosis in primary myelodysplastic syndromes: a retrospective study of 352 patients. 159 1

A previously healthy 16-year-old girl complaining of fever, hemosputum, chest pain and dyspnea was hospitalized. On admission, physical examination revealed mental confusion, holosystolic heart murmur, and swelling of the left foot. Laboratory investigations showed anemia, leukocytosis, thrombocytopenia, activation of inflammatory reactions, prolongation of PT and APTT, and hypoxia. Antinuclear antibody test was negative. There were no other findings suggestive of collagen diseases such as SLE. Chest X-ray showed consolidation in the left lower lung field and pleural effusion. Echocardiography disclosed a mass lesion in the left atrium in contact with the mitral valve, and mitral regurgitation. No findings indicative of an infectious etiology were present. The patient rapidly improved with high dose corticosteroid and anticoagulant therapy. A venogram of the lower extremity disclosed deep venous thrombosis. A lung ventilation-perfusion scan revealed multiple pulmonary thromboemboli. Elevation of anticardiolipin antibody was noted. Based on these findings, the diagnosis of primary antiphospholipid syndrome was made. Further administration of steroid and anticoagulant resulted in decrease of the titer of anticardiolipin antibody. This is the second report of primary antiphospholipid syndrome in Japan. The clinical significance of this disease is also discussed.
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PMID:[A case of primary antiphospholipid syndrome with fever, pulmonary thromboembolism and endocardial lesion]. 162 84

Hemostatic measurements were undertaken in eight chronic hemodialysis uremic patients on recombinant human erythropoietin (rHuEpo). Same measurements were repeated in another seven patients in whom anemia was corrected by the transfusion of red blood cells. The correction of the anemia by rHuEpo therapy was accompanied by 1. correction of the prolonged Simplate Bleeding Time (BT) to normal less than 10.0, minutes after 16 weeks of rHuEpo treatment; 2. significant increases in the levels of fibrinogen, clotting FVIII:C, vWF:antigen, vWF:ristocetin cofactor and platelet count; 3. enhanced aggregation responses to ADP, adrenaline, arachidonic acid, collagen and ristocetin. There was no significant fluctuation in other coagulation parameters PT, APTT, TT, reptilase time and antithrombin III and plasma fibrinogen. In patients who were treated with RBC transfusion and despite the correction of the anemia, the bleeding time shortened significantly but not corrected, mean BT before and after RBC transfusion was 17.1 +/- 1.4 and 11.6 +/- 1.9 minutes respectively. Besides there was significant elevation of vWF:Ricofactor levels but not FVIII:C, vWF:Ag or platelet count. Platelet aggregation responses to ADP remained unchanged. It is concluded that significant elevations of FVIII:related activities, plasma fibrinogen, improved platelet aggregability and correction of the BT are salient hemostatic changes that follow rHuEpo therapy in uremic patients.
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PMID:Effect of recombinant human erythropoietin (rHuEpo) on the hemostatic system in chronic hemodialysis patients. 175 76

Oxygen tension and collagen deposition were measured in standardized, subcutaneous wounds in 33 postoperative surgical patients. Pertinent clinical and wound parameters were analyzed by Pearson's correlation test and sequential linear regression analysis. Collagen deposition was directly and significantly proportional to wound oxygen tension and measures of perfusion. There were no significant correlations with hematocrit, estimated blood loss, length of operation, smoking, age, weight, sex, or urine output. This study in humans confirms animal experiments showing that collagen deposition and tensile strength in wounds are limited by perfusion and tissue oxygen tension. It appears unnecessary to maintain hemoglobin at normal levels to support repair, provided that peripheral perfusion can be maintained at a high level in compensation for anemia. These circumstances reflect the fact that although oxygen is essential to many aspects of healing, and must be delivered at adequate partial pressures, reparative tissue consumes relatively little of it.
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PMID:Tissue oxygenation, anemia, and perfusion in relation to wound healing in surgical patients. 195 14

Erythrocytes are known to influence hemostasis. Bleeding times are prolonged in anemia and corrected by normalizing the hematocrit. We now demonstrate that intact erythrocytes modulate biochemical and functional responsiveness of activated platelets. A two-stage procedure, permitting studies of cell-cell interactions and independently evaluating platelet activation and recruitment within 1 min of stimulation, was developed. Erythrocytes increased platelet serotonin release despite aspirin treatment, enzymatic adenosine diphosphate removal, protease inhibition, or combinations thereof. The data suggested that erythrocyte enhancement of platelet reactivity can reduce the therapeutic effectiveness of aspirin. Erythrocytes metabolically modified platelet arachidonate or eicosapentaenoate release and eicosanoid formation. They promoted significant increases in cyclooxygenase and lipoxygenase metabolites upon platelet stimulation with collagen or thrombin. However, with ionophore, erythrocytes strongly reduced platelet lipoxygenation. These erythrocyte modulatory effects were stimulus-specific. Activated platelet-erythrocyte mixtures, with or without aspirin, promoted 3-10-fold increases in extracellular free fatty acid, which would be available for transcellular metabolism. Erythrocyte-induced increases in free eicosapentaenoate may contribute to antithrombotic and anti-inflammatory effects of this fish oil derivative. These results provide biochemical insight into erythrocyte contributions to thrombosis and hemostasis, and support the concept of thrombus formation as a multicellular event.
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PMID:Enhancement of platelet reactivity and modulation of eicosanoid production by intact erythrocytes. A new approach to platelet activation and recruitment. 199 40


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