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)

In recent years, diagnostic imaging techniques, especially ultrasonography (US) and CT scanning, have been widely adopted in clinical practice, making early accurate diagnosis of renal tumors possible. A total of 452 cases of renal tumors have been admitted to the institute since 1951, of which 220 were seen from 1951 to 1979 and 232 in the past 9 years (1980-1988). The frequency of renal parenchymal tumors was obviously higher in the latter group, including asymptomatic renal carcinoma in 20.2% and hamartoma in 38.1%. All these were discovered on routine physical check-up by ultrasonography and/or CT scanning and would otherwise have gone undiagnosed on conventional urography. Ultrasonography and CT can also reveal the nature and the extent of the tumor. The idea that "a renal tumor should be considered malignant unless pathologically proven otherwise" is no longer valid. However, general manifestations of renal carcinoma, such as elevated erythrocyte sedimentation rate (ESR), hypertension, malaise, anemia, fever and hypercalcemia, still deserve proper attention. We suggest that ultrasonography of both kidneys should be mandatory in routine physical check-up, as far as the urinary system is concerned, in order to discover asymptomatic renal tumors.
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PMID:Imaging techniques for the diagnosis of renal tumors. 224 36

A patient with multiple, pyogenic hepatic abscesses is described, and the pathophysiology, etiologies, clinical and laboratory manifestations, and management of the disease are reviewed. A 55-year-old man with a history of ethanol abuse and pancreatitis developed fever, chills, general malaise, and right upper quadrant abdominal pain two weeks before hospitalization. Baseline laboratory and hematology results included serum albumin concentration, 3.2 g/dL; serum alkaline phosphatase concentration, 239 mIU/mL; total serum bilirubin concentration, 1.3 mg/dL; white blood cell count, 18,400/cu mm; red blood cell count, 4.7 million/cu mm; hemoglobin, 12.5 g/dL; and hematocrit, 38.8%. Abdominal ultrasound showed echo-free cavities throughout the hepatic parenchyma; abdominal computed-tomography (CT) scan showed hepatomegaly and multiple radiolucent spaces. CT-guided needle aspiration of a hepatic mass yielded purulent material that grew Fusobacterium necrophorum under anaerobic conditions. On day 7, the patient was started on i.v. ampicillin sodium-sulbactam sodium. A CT scan two weeks later showed a reduction in the number and sizes of abscesses. The patient continued i.v. therapy for one month, then was discharged on a regimen of p.o. amoxicillin trihydrate-clavulanate potassium. Hepatic abscesses are either amebic or pyogenic; the latter usually has a higher mortality. The etiologies of pyogenic hepatic abscesses include ascending cholangitis, portal vein bacteremia, systemic bacteremia, extension from a contiguous focus of infection, and trauma. Diagnosis is difficult and relies highly on clinical suspicion. Clinical symptoms include hepatomegaly, fever, chills, and malaise. Abnormal laboratory values include leukocytosis, anemia, and hypoalbuminemia. The abscesses are frequently polymicrobial; Escherichia coli is the most commonly isolated species. CT is the best radiological technique for diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ampicillin-sulbactam therapy for multiple pyogenic hepatic abscesses. 229 77

A phase I trial of 2-beta-D-ribofuranosylthiazole-4-carboxamide (NCS 286193, tiazofurin) was conducted using a 5-day i.v. bolus schedule, every 21 days. Thirty one patients with advanced cancer were entered on the trial. A total of 106 cycles were administered with doses ranging from 550 to 2750 mg/m2. Concomitant administration of Allopurinol was necessary to prevent hyperuricemia. Tiazofurin was difficult to evaluate and many side effects were variable and sporadic. The dose limiting toxicities were nonhematologic consisting particularly of myalgias, headaches and general malaise. Other toxicities included nausea, vomiting, stomatitis, lethargy, sleeping difficulty, sinus bradycardia, skin rash, desquamation of the palms and soles, photophobias and burning of the eyes. Hematologic toxicity was mild and not dose related though it led to a neutropenic septic death in one patient at 2750 mg/m2. Anemia was documented in 60% of cycles. Biochemical abnormalities consisted of mild hyperglycemia, hyperuricemia and elevated skeletal creatinine phosphokinase levels which did not correlate with the incidence or degree of myalgias. Though some patients were able to tolerate higher doses, the recommended dose for phase 2 study is 1650 mg/m2. Further studies will be required to achieve a better understanding of this interesting drug.
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PMID:Phase I study of tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide, NSC 286193). 238 15

Combined chemotherapy with cisplatin was performed in patients with advanced esophageal cancer. Two types of administration schedule were used: method I (three-drug combination of cisplatin, bleomycin and methotrexate) and method II (combination of cisplatin, peplomycin and methotrexate). Of 16 cases, 6 (37.5%) showed partial remission. With regard to the method of administration, the response rate for method I was 33%, and that for method II was 43%. Nausea (84%), vomiting (56%), loss of appetite (94%), malaise (75%) and alopecia (25%) were observed as side effects. Nausea and vomiting were ameliorated by use of metoclopramide. In bloodchemistry, anemia (87%), leukopenia (56%), thrombopenia (31%) and increase of BUN (63%) were observed. However, these changes were ameliorated by hydration or blood transfusion. Combined chemotherapy with CDDP should be a more useful future treatment for esophageal cancer.
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PMID:[Combined chemotherapy with cisplatin in esophageal cancer]. 244 65

The treatment of severe anemia related to end-stage renal disease with recombinant human erythropoietin (r-HuEPO; EPOGEN, [epoetin alfa] AMGEN Inc, Thousand Oaks, CA) has been investigated in more than 1,500 hemodialysis patients worldwide. The goal of r-HuEPO therapy is to maintain the hematocrit level at 35%, with a recommended starting dose of 150 mg/kg of body weight, administered intravenously after each dialysis three times a week for 6 to 12 weeks. Hematocrit levels should be measured at least once a week and the dose adjusted in increments or decrements of 10 mg/kg to 25 mg/kg to keep the hematocrit level between 33% and 40%. Patients receiving r-HuEPO must be normotensive. A history of seizures has been cause for exclusion from clinical trials. Patients' iron status should also be adequate at the onset of therapy, which is defined as a serum ferritin level of 100 ng/mL or more, and a transferrin saturation of more than 20%. Iron status and BP must be carefully monitored, and abnormalities corrected with iron supplementation, ultrafiltration, or antihypertensive medication. The lack of controlled studies makes determination of the actual incidence of side effects difficult, but it appears to be minimal. Possible side effects of r-HuEPO therapy include hypertension, seizures, myalgia, malaise, headache, gastrointestinal distress, and injected conjunctiva. The major benefits of r-HuEPO therapy are reduced need for transfusion and marked improvement in quality-of-life parameters.
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PMID:Who should receive recombinant human erythropoietin? 266 84

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

Clinical details and present day problems encountered in 425 cases of falciparum malaria (PF) are reported. 10.11% had taken chloroquine prior to reporting to us. Parasitic count done in 23.05% cases lacked correlation with severity of disease. Pattern of fever varied markedly but 5.4% were afebrile throughout and presented only with bodyache and malaise. Apyrexial spell was noted in 5.64%. 28.70% had typical facial looks of anaemia and sallow complexion. Cerebral symptoms were noted in 3.05%. Other symptoms were severe headache 33.4%, pain abdomen 3.29%, gastroenteritis 5.64%, jaundice 2.58% and bronchitis in 7.50%. We encountered subconjunctival haemorrhages with purpura and/or urticaria in four cases, symptoms suggestive of shock lung in 3, pulmonary oedema in 2, severe anaemia (HB less than 4 g%) in seven pregnant ladies, extrapyramidal symptoms in follow up period in 5 and congenital malaria in 2 cases. 83.25% were cured with chloroquine and oxytetracycline. 8.47% (who deteriorated despite the above treatment) were treated with quinine for 6 days. 5.17% (with severe disease) were also given quinine as first line drug. 2.82% (unresponsive to chloroquine and oxytetracycline but with mild disease) were treated with pyrimethamine-sulphamezathine combination for 5 days. One case who did not respond to quinine was treated with quinidine. Recrudescence was seen in 3.67% of patients treated with chloroquine and oxytetracycline. There was no case with renal failure, haemolysis due to G6PD deficiency and black water fever. There was only one death (0.23%) in our series. Self-medication, haphazard therapy and the slogan "Fever may be malaria-take chloroquine" can lead to problems in falciparum malaria.
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PMID:Falciparum malaria--present day problems. An experience with 425 cases. 269 36

Clinical, hematologic and hemoglobin composition data on the first case of Hb 0-Arab in association with beta 0-thalassemia in Yugoslavia are reported here. The propositus was a 26-years-old female from Strumica who was admitted to the hospital for several times because of anemia, hepatosplenomegaly, occasional abdominal pains, malaise and fatigue. Laboratory results presented: Hb 10.0 g/dl, RBC 3.84.10(12)/L, PCV 0.260 l/l, MCV 68 fl, MCH 26 pg, reticulocyte count 1.8%, anisopoikilocytosis, polychromasis, numerous target cells, total bilirubin 2.1 mg/dl, (indirect 1.7 mg/dl), serum-Fe 32.3 microM/L. A starch gel electrophoresis of hemolysate provided evidence for the presence of abnormal hemoglobin (approximately 85%) and Hb F (approximately 15%); the Hb A was absent. Familial screening showed her father was heterozygous for the abnormal hemoglobin, whereas the mother was heterozygous for beta-thalassemia. In vitro biosynthesis disclosed a total absence of beta globin and reduced synthesis of beta x x and gamma globin. The alpha/beta x + gamma-globin ratio was 1.77 (normal, 1.0 + 0.1). Amino acid analysis revealed that lysine substituted for glutamic acid at the position one hundred twenty-one of the beta chain (= Hb 0-Arab or beta 121 Glu----Lys).
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PMID:[Hemoglobin O Arab in interaction with beta 0-thalassemia]. 273 98

Brequinar sodium is a 4-quinolinecarboxylic acid analogue that inhibits dihydroorotate dehydrogenase and subsequent de novo pyrimidine biosynthesis. It has shown dose-dependent antineoplastic activity against several mouse and human tumor models. This trial evaluated Brequinar given as a single daily i.v. bolus over a 5-day period repeated every 28 days. One hundred seven courses of treatment at dosages ranging from 36 to 300 mg/m2/day x 5 were administered to 45 patients (31 male and 14 female) with refractory solid tumors; median age was 58 years (range 30-74); median Southwest Oncology Group performance status was 1 (range, 0-3). Thirty patients had prior cytotoxic chemotherapy. Dose-limiting toxicities were thrombocytopenia and a severe desquamative maculopapular dermatitis. Two of 5 good risk patients at 300 mg/m2 and 3 of 6 poor risk patients at 170 mg/m2 developed a platelet count less than 25 x 10(3)/microliters. Two of 5 good risk patients at 300 mg/m2 and 1 of 6 poor risk patients at 170 mg/m2 developed a severe desquamative dermatitis. Moderate to severe mucositis was usually associated with the thrombocytopenia and/or the dermatitis. Nonhematological drug-related toxicities included nausea and vomiting, malaise, anorexia, diarrhea, phlebitis, reversible transaminase elevation, and mucositis. Other hematological toxicities were anemia, granulocytopenia, and leukopenia. There were no drug-related deaths. There were no objective tumor responses. Plasma and urine levels of Brequinar were quantified by high pressure liquid chromatography in 28 patients. Plasma levels and areas under the curve increased proportionally with increased dose. Brequinar had a harmonic mean terminal t1/2 of 8.1 +/- 3.6 h with a model-independent determined apparent volume of distribution at steady state of 9.0 +/- 2.9 liters/m2 and a total body clearance of 19.2 +/- 7.7 ml/min/m2. Renal excretion was a minor route of elimination for Brequinar. The maximally tolerated dose of Brequinar on a daily x 5 i.v. schedule was 250 mg/m2 for good risk patients. For the daily x 5 i.v. schedule, the recommended dose of Brequinar for phase II evaluation is 250 mg/m2 for good risk patients and 135 mg/m2 for poor risk patients.
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PMID:Phase I clinical and pharmacokinetic trial of Brequinar sodium (DuP 785; NSC 368390). 274 43

A case of AML accompanied by HTLV-I associated myelopathy (HAM) is reported. A 37-year-old woman was admitted to our hospital in April 1985 because of severe anemia, general malaise and fever. On admission, anemia, thrombocytopenia and leukocytosis consisting of 32% myeloblasts and 6% promyelocytes were noted. A bone marrow study revealed marked myeloid hyperplasia, and a diagnosis of acute myelogenous leukemia (M2) was made. In order to improve the patient's severe anemia and thrombocytopenia, a large amount of blood transfusion was applied at once. Thereafter BHAC-DMP therapy was commenced resulting in complete remission 3 months after initiating chemotherapy. Hematological improvement has continued (as of May 1988). In June 1986 the patient showed a gait disturbance of slowly progressive course. Neurological examination revealed hyperactive knee and ankle jerks with a positive Babinski's sign, and foot clonus were also noted bilaterally. Sphincter impairment was detected. A CSF sample contained slight pleocytosis with some abnormal lymphocytes similar to those found in adult T cell leukemia. Antibodies to HTLV-I were found in the CSF and serum by EIA method. According to these findings we diagnosed the patient's illness as HAM, referring to the new clinical entity named by Osame. This patient had undergone a blood transfusion 14 months before the onset of this myelopathy, therefore the transmission of exogenous antigens through blood transfusion may be the cause of HAM. Corticosteroid pulse treatment was administered and striking improvements countering gait disturbance resulted in this patient.
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PMID:[Acute myelogenous leukemia accompanied by HTLV-I associated myelopathy (HAM) caused by blood transfusion]. 274 79


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