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)

Seventeen patients had spontaneous orbital hemorrhages. The usual symptoms were acute onset of pain, proptosis, and vomiting with decreased vision, limitation of motility, and ecchymosis of the eyelids occurring in some patients. The children often developed a progressive space occupying lesion that simulated a neoplasm. Most patients had underlying venous anomalies, although several elderly patients with atherosclerosis developed arterial hemorrhages with more abrupt and dramatic symptoms. Other associated conditions included hypertension, anemia, labor, and von Willebrand's disease. The visual outcome was good except in the elderly patients, half of whom had severe and permanent visual loss.
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PMID:Orbital hemorrhage. 47 97

The authors have identified six Southeast Asian patients ranging in age from 14 to 21 years with hemoglobin E-beta(0) thalassemia and a coagulopathy involving von Willebrand factor (vWF). These patients had normal or only slightly decreased plasma clotting factor levels. The activated partial thromboplastin time was prolonged in four of the patients. The abnormal feature common to all patients was a qualitative loss of high molecular weight multimers of vWF by crossed immunoelectrophoresis (vWF:CIE). Plasma vWF antigen concentration (vWF:Ag) and ristocetin cofactor activity (vWF:RCo) also were decreased and bleeding time prolonged in three patients. Epistaxis was present in two. No family history of increased bleeding tendency was present in any patient. Coagulation parameters and vWF:CIE were normal in two first-degree relatives without this hemoglobinopathy. vWF abnormalities and clinical manifestations were greatest in those patients with the most severe anemia and hepatosplenomegaly. These six patients appear to have an acquired abnormality of vWF, although they lack the clinical characteristics of acquired von Willebrand disease. While the etiology of this abnormality is unclear, the authors speculate that proteolysis of vWF secondary to extramedullary hematopoiesis or loss through high cardiac output shear stress in these anemic patients may be involved.
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PMID:Abnormality of von Willebrand factor in patients with hemoglobin E-beta (0) thalassemia. 210 77

A 17 year old woman presented with severe anaemia due to menorrhagia. On investigation, she was shown to have abnormalities of her haemostatic mechanism consistent with von Willebrand's disease Type I, although there was no family history of this disorder. In addition, she was shown to have severe primary hypothyroidism. On correction of hypothyroidism with oral thyroxine, her coagulation defects returned to normal and menorrhagia ceased. This is consistent with acquired von Willebrand's disease secondary to hypothyroidism.
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PMID:Acquired von Willebrand's disease and hypothyroidism: report of a case presenting with menorrhagia. 221

A new case of acquired von Willebrand syndrome (AvWS) with Hashitoxicosis and pernicious anemia combined in a 73-years-old male is reported. He was admitted because of appetite loss and general malaise. Physical examination showed severe anemia and general edema. The red-cell count was 103 X 10(4)/microliters with a MCV of 122 fl; the white-cell count was 2,900/microliters with 24.5% hypersegmented neutrophils; the platelet count was 17.2 X 10(4)/microliters. the lactate dehydrogenase was 9,513 U/ml and vitamin B12 was 87 pg/dl. An aspirated specimen of bone marrow was diagnostic of megaloblastic anemia. The thyroid hormones were decreased with the thyroid stimulating hormone increased. From the immunological findings, the thyroid-test, microsome-test, and anti-intrinsic factor were positive, but M proteinemia and Bence Jones proteinuria were absent. Histology of the thyroid gland and the gastric mucosa established the diagnosis of chronic thyroiditis and chronic atrophic gastritis. Subcutaneous hemorrhages after veni-puncture were observed on admission. He had a normal bleeding time, but the coagulation studies indicated the presence of von Willebrand disease, but as his family and past history were negative, this suggested the presence of an AvWS. The analysis of von Willebrand factor (vWF) multimeric composition had showed the lack of the larger multimers in the plasma, but it was normalized after the administration of levothyroxine sodium and hydroxocobalamin with vWF: Ag/RCo ratio paralleled. As far as we know, this is the first report of AvWS with Hashitoxicosis and pernicious anemia combined.
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PMID:[Acquired von Willebrand syndrome associated with Hashitoxicosis and pernicious anemia combined]. 267 35

A 62 year old male (R.H.) presented with a mild anemia (Hb 11-12 gm%) and a history of multiple hemorrhagic episodes. The marrow had 40-50% sideroblasts. Marrow chromosomes were normal. His wife was hematologically normal, while one daughter, age 30 years, had a sideroblastic anemia (Hb 11-12 gm%) with 40-50% sideroblasts in the marrow. Her anemia was first noted at age 15 years. Administration of vitamin B6 did not correct the anemia in either the father or daughter. Platelet abnormalities inherited jointly with this disorder are described for the first time. Both R.H. and his daughter had prolonged bleeding times, with normal PTT, PT times, fVIII:C, fVIII:Ag levels, and vWF multimers, which may rule out a von Willebrand's disease. They have normal platelet numbers but abnormally low platelet adhesiveness and greatly depressed ADP, collagen, and epinephrine responsiveness. Response to ristocetin was in the low normal range, and aggregation with thrombin was normal. While desmopressin completely normalized R.H.'s bleeding time, none of these platelet parameters were improved. No differences in the SDS PAGE protein patterns of RH platelets could be detected in comparison to normal samples. His platelets took up and released serotonin (5HT) normally, and electron micrographs defined no morphological abnormalities. However, no ATP was released from platelets activated with collagen, and when followed by thrombin about fourfold greater ATP was released by control platelets as compared to RH platelets. The dense granule fraction derived from RH platelets contained about 20% the level of ATP, 40% the level of ADP, and 50% the level of 5HT detected in a normal sample. The results indicate that the bleeding disorder is related to a non-classical heritable storage pool defect. The connection between the inherited sideroblastic anemia and platelet defects is obscure.
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PMID:Hereditary sideroblastic anemia with associated platelet abnormalities. 281 25

A bleeding disorder (von Willebrand's disease) was diagnosed in a 9-year-old male Himalayan cat examined because of persistent oral bleeding after routine dental extraction. Bleeding subsided after empirical treatment, which included prednisolone, vitamin K1, and transfusion of fresh blood, but recurred spontaneously after 8 months of apparent good health. Pertinent results of routine laboratory testing included an inconstant prolongation of the activated partial thromboplastin time and recurring iron-deficiency anemia. Assays of specific coagulation factors revealed low factor VIII coagulant activity and undetectable factor VIII-related antigen, a pattern considered to be diagnostic of von Willebrand's disease. This condition, not previously reported in a cat, should be included in the differential diagnosis when cats are examined because of abnormal bleeding.
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PMID:A bleeding disorder (von Willebrand's disease) in a Himalayan cat. 310 51

Antiplatelet therapy is known to be beneficial in reducing the incidence of transient ischemic attacks and cerebral infarctions in nonsickling populations. We report two siblings with homozygous sickle-disease and von Willebrand's disease who had recurrent cerebral infarctions (stokes) and transient ischemic attacks despite an inherent inhibitory platelet effect from their vWd and antiplatelet therapy. The development of stroke in patients with sickle hemoglobinopathies and the possible role of platelets and antiplatelet therapy in cerebrovascular accidents in sickle-cell anemia are discussed.
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PMID:Recurrent strokes in two siblings with sickle-cell disease and von Willebrand's disease: implications of the role of platelets. 315 68

Lipomas of the digestive tract are rare and may give rise to obstruction, intussusception or haemorrhage. In a 74-year old woman with Von Willebrand's disease, a lipoma in the ileocaecal valve caused frequent intestinal haemorrhages and chronic anaemia over a period of more than 15 years. Diagnosis and therapy are discussed on the basis of the case history.
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PMID:Recurrent intestinal haemorrhages caused by a lipoma in the ileocaecal valve in a patient with Von Willebrand's disease. 697 Mar 51

In 1994, the American Society of Anesthesiologists established the Task Force on Blood Component Therapy to develop evidence-based indications for transfusing red blood cells, platelets, fresh-frozen plasma, and cryoprecipitate in perioperative and peripartum settings. The guidelines were developed according to an explicit methodology. The principal conclusions of the task force are that red blood cell transfusions should not be dictated by a single hemoglobin "trigger" but instead should be based on the patient's risks of developing complications of inadequate oxygenation. Red blood cell transfusion is rarely indicated when the hemoglobin concentration is greater than 10 g/dL and is almost always indicated when it is less than 6 g/dL. The indications for autologous transfusion may be more liberal than for allogeneic (homologous) transfusion. The risks of bleeding in surgical and obstetric patients are determined by the extent and type of surgery, the ability to control bleeding, the actual and anticipated rate of bleeding and the consequences of uncontrolled bleeding. Prophylactic platelet transfusion is ineffective when thrombocytopenia is due to increased platelet destruction. Surgical and obstetric patients with microvascular bleeding usually require platelet transfusion if the platelet count is less than 50 times 10(9)/l and rarely therapy if it is greater than 100 times 10(9)/l. Fresh-frozen plasma is indicated for urgent reversal of warfarin therapy, correction of known coagulation factor deficiencies for which specific concentrates are unavailable, and correction of microvascular bleeding when prothrombin and partial thromboplastin times are >1.5 times normal. It is contraindicated for augmentation of plasma volume or albumin concentration. Cryoprecipitate should be considered for patients with von Willebrand's disease unresponsive to desmopressin, bleeding patients with von Willebrand's disease, and bleeding patients with fibrinogen levels below 80-100 mg/dL. The task force recommends careful adherence to proper indications for blood component therapy to reduce the risks of transfusion. (Key words:Practice guide-lines: anemia: blood component therapy; coagulopathy; cryoprecipitate; fresh-frozen plasma; red blood cells; transfusion.)
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PMID:Practice Guidelines for blood component therapy: A report by the American Society of Anesthesiologists Task Force on Blood Component Therapy. 871 70

Angiodysplasic lesions can be located anywhere in the gastrointestinal tract, but most of them are found in the cecum and right colon. Angiodysplasias are very infrequent in the stomach and small bowel. These lesions can be associated with several clinical conditions, such as certain coagulation disorders and liver diseases. We report the case of a diffuse gastrointestinal angiodysplasia in a female patient with idiopathic cirrhosis of the liver who developed a coagulopathy which mimicked von Willebrand disease. After repeated blood transfusions, which were not able to control the anemia of the patient, an antrectomy was performed because most lesions were located in the antrum. The procedure did not achieve a suitable control of the bleeding. Finally, a hormonal therapy combining estrogens and progestagens, was able to control, at least partially, the patient's chronic gastrointestinal bleeding.
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PMID:[Diffuse gastrointestinal angiodysplasia associated with cryptogenic hepatic cirrhosis and coagulopathy simulating von Willebrand disease]. 896 79


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