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 initial clinical phase I trial of inosine dialdehyde has been carried out in 40 patients at dose levels of 30-4000 mg/m2 for 5 days given intravenously (iv) monthly. At 1.5 g/m2, noncumulative dose-related toxicity occurred in all patients which consisted of nausea and vomiting, local pain, alterations in coagulation mechanism, elevated partial thromboplastin time, and positive Coombs' test. No dose-limiting leukopenia, thrombocytopenia, anemia, or bleeding occurred; however, depression of the leukocyte and platelet counts, and decreased hemoglobin value were observed. The dose-limiting toxic effect was renal tubular damage with reversible acute renal failure in one of four patients who received 3000 mg/m2 iv for 5 days. Refractory hypercalcemia was controlled in three of three patients without tumor effect. Responses occurred in patients with seminoma, oat cell carcinoma, and melanoma. A starting dose of 2 g/m2 for 3 days monthly is recommended for phase II trials and a trial in lung carcinoma is now being conducted.
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PMID:Clinical phase I trial of inosine dialdehyde (NSC-118994). 110 41

This report reviews the manifestations in fifteen children of proved adenoviral pneumonia. Patients' ages ranged from 43 days to 4 years and 1 month. Twelve cases were younger than 2 years old. Adenoviral infections were proved by positive viral cultures or a four-fold increase of the complement fixation titer. Prolonged fever and cough were found in all cases. In 13 patients, respiratory distress occurred; 5 needed mechanical ventilation. Injected throats, conjunctivae and ear drums were common. Other clinical pictures included abdominal discomfort, hepatomegaly, skin rash, convulsion and bleeding tendency. Abnormal laboratory findings were mild anemia, leukopenia, thrombocytopenia, elevated erythrocyte sedimentation rate and C-reactive protein, impaired liver function test, and prolonged prothrombin time and partial thromboplastin time. Anemia (11 cases), leukopenia (7 cases) and elevated transaminases levels (7 cases) were more common than previously reported. All patients had para-hilar peribronchial infiltrates in chest roentgenography. Segmental atelectasis and compensated hyper-expansion were found frequently. Pleural effusion were noted in six of our cases. Air leak syndrome occurred in three patients who had received mechanical ventilation. Three of the 15 patients expired: one had a preceding measles infection, all had disseminated intravascular coagulopathy. For patients with antibiotic-resistant pneumonia, adenoviral studies should be done. Extrapulmonary manifestations, and some abnormal laboratory findings, i.e., mild anemia, leukopenia, impaired liver function are clues to adenoviral infections, while bleeding tendency can be regarded as a poor prognostic sign for children with adenoviral pneumonia.
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PMID:Adenoviral pneumonia in children. 132 94

A variant strain of Rauscher leukemia virus (RLV-A) obtained from a transplantable murine monomyelocytic leukemia causes a disease characterized by frank anemia, wasting, hepatosplenomegaly and erythroblastosis. The involvement of platelets in this disease are reported here. The RLV-A induced a severe thrombocytopenia (25 percent of control level) at the terminal stage of disease. This thrombocytopenia was not associated with disseminated intravascular coagulopathy since the prothrombin times were always within normal limits. The partial thromboplastin time was elevated in the terminal stages of disease and was found to be associated with factor deficiencies, possibly owing to the presence of anti-factor antibodies, in the intrinsic coagulation pathway, especially factor VIII. Further, splenectomy did not abolish the thrombocytopenia, since splenectomized, virally infected animals also developed severe thrombocytopenia (29 percent of control levels). The ensuing splenomegaly during progression of disease was not the cause of the thrombocytopenia. A physiological response to the severe thrombocytopenia was the production of larger size platelets. At terminal stages of the disease, platelet volume increased to 4.2 mu 3 (normal is 3.0 mu 3). An increase in platelet volume was also observed in splenectomized, virally infected animals. Electron microscopy indicated that these circulating platelets contained c-type viral particles. Viral infection was associated with decreased life span of circulating platelets, as measured by 75Se-methionine at mid and terminal stages of the disease. Our results suggest that direct viral infection of platelets and/or megakaryocytes with subsequent cell lysis is a possible cause of the observed thrombocytopenia observed in RLVA-induced disease and may also occur in other retrovirally-induced diseases.
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PMID:Thrombocytopenia in a retrovirally-induced murine erythroleukemia. 145 28

The hemostatic effects of recombinant human erythropoietin (rHuEP) were investigated in 20 patients with end-stage renal disease (thirteen on hemodialysis, seven without dialysis) receiving this hormone. We studied their hemograms and coagulation profiles before and at 1 month after initiation of rHuEP therapy. One month after rHuEP administration, improvement in anemia (16/20, 80%) and shortening of bleeding time (17/19, 89.5%) were observed. Shortening or correction of bleeding time was achieved in three patients without any increase of the hemoglobin level. This means that factors other than the increased hematocrit level might contribute to shortening bleeding time in uremic patients receiving rHuEP treatment. The platelet count, prothrombin time, partial thromboplastin time, and fibrinogen level did not change over the course of rHuEP therapy. Thrombosis of vascular access was not observed, and heparin doses were not increased in this short-term period. A significant decrease was found in the plasminogen level, from 108.5% to 88.2% (p less than 0.05), in uremic patients on hemodialysis. The antithrombin III level also decreased, from 98.8% to 89.8% (p less than 0.05), and its level dropped to below normal ranges in six of thirteen patients (46%) on hemodialysis after treatment with rHuEP. No significant change was noted in the levels of antithrombin III, plasminogen, and alpha 2-antiplasmin in uremic patients not receiving dialysis. These results suggest that rHuEP administration induces increased extracorporeal dialyzer clotting and consumption coagulopathy, and that this extracorporeal consumption coagulopathy may play a role in the genesis of thrombotic complications.
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PMID:The effect of recombinant human erythropoietin on hemostatic status in chronic uremic patients. 151 Nov 68

Two cases of the severe form of meningococcal infection are described. A 17-year-old girl and a (unrelated) 2-year-old boy suddenly developed fever and rigor. Several hours later petechiae of the skin were noted: they rapidly spread. On admission the girl was found to have a severe consumptive coagulopathy (prothrombin 24%, partial thromboplastin time 104 sec, fibrinogen 73 mg/dl, platelets 35,000/microliters). She died two-and-a-half hours after admission of treatment-resistant shock. The boy had at first only a low prothrombin value (39%), but later the other coagulation values also became abnormal. He died 16 hours after admission from the consumptive coagulopathy and profound anaemia (haemoglobin 7.4 g/dl, haematocrit 0.23). Neither patient had any clinical signs of meningitis. Isolation of Neisseria meningitidis from blood cultures confirmed the diagnosis.
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PMID:[Therapy-refractory fulminant meningococcal sepsis]. 190 44

Eighty-two women whose pregnancy was complicated by anemias of varying severity and twelve healthy pregnant women were examined. Blood plasma immunoglobulins A, G, and M were measured by immunochemical methods, as were the immune complexes of various levels and some parameters of the homeostasis system. The findings evidence a noticeable elevation of the concentrations of all immunoglobulins, of low-disperse immune aggregates in severe anemia of pregnancy, as well as intensive synthesis of immunoglobulin M in the fetus, low level of large immune complexes, and stimulation of some homeostasis components that results in consumption coagulopathy and chronic DIC syndrome. Correlations between some parameters of the blood coagulation and fibrinolysis systems, on the one hand, and humoral immunity characteristics, on the other, may be traced, among these correlations being reverse correlations between IgG level, activated recalcification time, fibrinogen concentration, and activated partial thromboplastin time.
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PMID:[Various factors of nonspecific resistance in pregnant women with anemia]. 195 69

Four patients with primary pulmonary hypertension, microangiopathic hemolysis, and thrombocytopenia were seen at the Charleston (WVa) Area Medical Center between 1983 and 1988. Characteristic laboratory and clinical features of these patients were the following: mild anemia, reticulocytosis, low serum haptoglobin value, microangiopathic red blood cell changes on peripheral blood smear, mild to moderate thrombocytopenia, normal clotting studies (ie, prothrombin time, partial thromboplastin time, fibrinogen), negative direct Coombs' test, negative glucose water test, normal serum urea nitrogen and creatinine levels, lack of improvement of hemolysis and thrombocytopenia in response to vasodilators or calcium channel blockers, and severe plexiform lesions in the pulmonary vasculature with fibrin deposition at autopsy. The hemolysis and thrombocytopenia probably developed as a result of flow through the fibrin deposition in the plexiform lesions in the pulmonary circulation and subsequent shearing of red blood cells and platelets.
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PMID:Primary pulmonary hypertension. Its association with microangiopathic hemolytic anemia and thrombocytopenia. 204 24

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

The routine preoperative evaluation of pediatric patients often includes a history, physical examination, complete blood count, and urinalysis (UA). We retrospectively reviewed the records of 486 elective surgeries in children to determine the role of abnormal preoperative laboratory test results in perioperative management. Anemia or microcytosis was apparent in 17% of patients, and abnormal UA results were found in 15%. More than 80% of the abnormal UA results were historically known, clinically insignificant, or false-positives. Only five children had surgery canceled owing to abnormal laboratory tests: two owing to anemia, two to an abnormal UA, and one because of a prolonged partial thromboplastin time. Both children with anemia were treated with iron and subsequently underwent surgery without complication. Of the abnormal UAs, one was contaminated, and the cancellation of surgery resulted in a complication requiring emergency surgery. The other abnormal UA was a probable asymptomatic bacteriuria, and the infant later underwent surgery uneventfully. These data suggest that a routine UA adds little to the preoperative evaluation of a healthy child, and should be omitted.
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PMID:Preoperative laboratory testing of children undergoing elective surgery. 230 50

A case is reported of a 60 year-old patient with chronic disseminated intravascular coagulation (DIC) which was increased by the therapeutic embolization of a renal tumour. The patient had 2 primary carcinomas (renal and prostatic) with vertebral metastases, severe chronic anaemia (due to haematuria), and chronic DIC, with thrombocytopaenia, soluble complexes, and fibrinogen and fibrin degradation products. Therapeutic embolization of the renal artery was carried out with fragments of dura mater. Although the result was anatomically very satisfactory, the patient's condition worsened, with continuing haematuria, and development of an haematoma in the lumbar fossa. Coagulation factors and antithrombin III (AT III) concentrations decreased, whereas the activated partial thromboplastin, thrombin and reptilase times increased. The patient also suffered from acute renal failure (creatinine: 690 mumol.l-1). Treatment consisted in fluid replacement, red blood cell and platelet transfusions, 150 IU.kg-1.d-1 heparin and 20 IU.kg-1.d-1 AT III. Haematological tests returned to pre-embolization values on the ninth day. The sudden worsening in the patient's condition was probably due to the sudden massive release of tissue thromboplastins related to the renal necrosis induced by the therapeutic embolization. The use of heparin AT III in the management of this patient is discussed.
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PMID:[Worsening of chronic disseminated intravascular coagulation after embolization of the renal artery]. 233 Oct 88


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