Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following a three-week administration of alpha-interferon (IFN-alpha), a 62-year-old woman with chronic hepatitis C manifested fever and dyspnea and showed diffuse infiltrative opacities on chest roentgenograms. Her laboratory data included results of anemia with reticulocytosis, a decreased complement level and hepatitis with elevated ALP, LDH and gamma-GTP. Because laboratory data also revealed a positive lymphocyte stimulation test for IFN-alpha, this cytokine was considered to be responsible for the development of interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction due to its immunomodulatory effects. Although these three disorders have been reported to develop singly after IFN-alpha therapy, this is the first report of a patient in whom these disorders occurred simultaneously.
 ...
PMID:A patient with chronic hepatitis C who simultaneously developed interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction after alpha-interferon administration. 791 19

A 49-year-old man was admitted to our hospital for dyspnea. Chest X-ray examination showed a massive right pleural effusion. Using intrathoracic tube drainage, a large quantity of chocolate-like pleural effusion was removed. Laboratory data demonstrated severe anemia and hypoproteinemia, and TPHA was positive. Antiameba antibody in blood was high, and a liver abscess was demonstrated on abdominal CT scan. Amebic liver abscess and amebic empyema were thus diagnosed. With pleural tube drainage and percutaneous liver abscess drainage, metronidazole (1.5 g/day) was administered. After administering this drug, the high temperature normalized and the patient's general condition improved significantly. Recently, amebic infections have been reported in increased numbers, especially in male homosexuals and immunocompromised patients. Henceforth amebic infection should be considered when pleural effusion and empyema are suspected.
 ...
PMID:[Amebic empyema, a case report]. 796 49

A 54 year-old woman who had a 6 month history of polyarthralgias, oral ulcers, weight loss and fatigue was admitted to the Urawa Municipal Hospital. She developed high fever, dyspnea and thrombocytopenia. Chest radiograph revealed massive right pleural effusion. At this time, laboratory investigations gave the following results: hemoglobin 12.7 g/dl, WBC 7700/microliters and platelet count 9.2 x 10(4)/microliters. Antibody to DNA was negative. Antinuclear antibody was positive at a titer of 320x in a centromere pattern; Anti-RNP and anti-Sm antibodies were negative. CH50 was 18.6 u/ml. C3 was 42.9 mg/dl. C4 was 11.5 mg/dl. Circulating immune complex (Clq) was 30.5 micrograms/ml. Circulating lupus anti-coagulant and anticardiolipine antibodies were positive. Thoracocentesis was performed; the material was a straw-colored exudate with over two thousands white cell per ul and showed marked reduction of complement titiers and elevated immune complex levels. She was then diagnosis as having SLE. Two weeks after admission, progressive leukopenia and anemia succeedingly occurred and resulted in severe pancytopenia. Bone marrow biopsy demonstrated marked marrow fibrosis and increased reticulin content with no evidence of malignancy. Steroid pulse therapy for 3 days started, and subsequently she was treated with 60 mg/day of prednisolone. Three weeks after starting on steroids, the massive pleural effusion was completely disappeared and complement titiers were normalized. Circulating immune complex has not been detected any more. After 8 weeks, the peripheral blood count was normalized. The dose of prednisolone was reduced progressively. On this occasion, the biopsy showed normocullular marrow with a marked reduction in the amount of reticulin.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[A case of systemic lupus erythematosus presenting with myelofibrosis as a cause of pancytopenia]. 797 29

Xylene is an aromatic hydrocarbon widely used in industry and medical technology as a solvent. Health and safety authorities in most countries, including Australia, recommend a threshold limit value (TLV) of 100 ppm in the working environment. Recently, the amount of the major metabolite of xylene, methylhippuric acid (MHA), in urine has been recommended as a better indicator of exposure. The American Conference of Governmental Industrial Hygienists has recommended an upper limit for this indicator, called a biological exposure index (BEI), of 2.0 g MHA/L urine (SG 1.016). Xylene vapour is absorbed rapidly from the lungs, and xylene liquid and vapour are absorbed slowly through the skin. Of the xylene absorbed, about 95% is metabolised in the liver to MHA and 70 to 80% of metabolites are excreted in the urine within 24 hours. However, the many variables which affect the absorption, metabolism and clearance of xylene include exercise, alcohol intake, cigarette smoking, co-exposure to other solvents, gender, and gastrointestinal, hepatic and renal pathology. Xylene in high concentrations acts as a narcotic, inducing neuropsychological and neurophysiological dysfunction. Respiratory tract symptoms are also frequent. More chronic, occupational exposure has been associated with anemia, thrombocytopenia, leukopenia, chest pain with ECG abnormalities, dyspnea and cyanosis, in addition to CNS symptoms. Concomitant exposure to xylene and other solvents, including toluene, affected hematological parameters, liver size, liver enzymes, auditory memory, visual abstraction, and vibration threshold in the toes. Normal metabolic pathways were altered and significant increases in some serum bile acids may reflect early liver damage.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Xylene: its toxicity, measurement of exposure levels, absorption, metabolism and clearance. 799 Dec 89

In a phase I trial, 17 patients were treated with 5-fluorouracil (5-FU) 500 mg/m2 and leucovorin (LV) 500 mg/m2 intravenously weekly for 6 weeks followed by 2 weeks' rest and interferon alfa-2b 1, 3, 5, 8, or 10 million units (MU) subcutaneously tiw with no rest period. The most common toxicities were fatigue (12), diarrhea (10), nausea/vomiting (7), and fever (7). The maximum tolerated interferon dose was 8 MU tiw. Fatigue and increased incidence of other toxicities rather than a single dose-limiting toxicity occurred at the next highest interferon level. ECOG grade III/IV toxicity occurred in 5 patients and included transient supraventricular tachycardia and brief seizure episode (1), dyspnea (1), decreased performance status (1), anemia requiring transfusion (1), and deep vein thrombosis (1). No toxic deaths occurred. Two patients with non-small cell lung cancer (NSCLC) had partial responses lasting 5 and 4 months. Two other patients with NSCLC had either minor response or stable disease, and 1 patient with colon cancer had a significant decline in serum CEA. The recommended alpha interferon dose is 8 MU tiw when given with this schedule of 5-FU/LV.
 ...
PMID:Alpha interferon, leucovorin, and 5-fluorouracil (ALF) in advanced cancer: results of a dose-finding study and evidence of activity in non-small cell lung cancer. 803 55

Between January 1980 and December 1990, 75 (57.3%) of 131 patients with metastatic gestational trophoblastic tumor had pulmonary metastases detected on plain chest roentgenography at the King Faisal Specialist Hospital and Research Centre. Pulmonary involvement was commonly extensive, with 32 (42.7%) patients having > 10 pulmonary metastases and 45 (60%) patients having a pulmonary lesion > 5 cm in diameter. Greater than 50% lung opacification, mediastinal involvement and pleural effusion were present in 25 (33.3%), 25 (33.3%) and 36 (48%) patients, respectively. Eight (10.7%) patients developed early respiratory failure requiring mechanical ventilation within one month of presentation. The development of early respiratory failure was significantly associated with the presence of dyspnea, anemia, clinical pulmonary hypertension, cyanosis, > 50% lung opacification, mediastinal involvement and bilateral pleural effusion. Because all patients requiring mechanical ventilation died, the use of extracorporeal perfusion should be considered in patients with early respiratory failure.
 ...
PMID:Pulmonary metastases of gestational trophoblastic tumor. Risk factors for early respiratory failure. 803 73

A reduction in the capacity of blood to carry oxygen leads to increased extraction of oxygen from the blood by peripheral tissues, and consequently to a decrease in the venous partial pressure of oxygen (pO2). At reduced venous pO2 pre-existing venous-arterial shunts gain in influence on arterial pO2 and arterial pO2 also decreases. In addition, physical exercise leads to lactate acidosis earlier and at lower levels of exercise than in healthy subjects. The low arterial pO2 and the low pH of acidosis are sensed by chemoreceptors of the carotid bodies and neural signals are transmitted to centers of the brain stem, where they are integrated and result in the sensation of shortness of breath (dyspnea). The capacity of the blood to carry oxygen is determined not only by the concentration of hemoglobin but also by the binding characteristics of hemoglobin for oxygen, which can be deduced from its molecular structure. In contrast to cases with acute anemia, dyspnea is often absent in patients in whom anemia develops gradually (down to hemoglobin levels of 7 g/dl). This tolerance is not mediated by pulmonary or cardiac compensatory mechanisms also at work in acute anemia, but is due to increases in the concentration of diphosphoglycerate. This allosteric effector molecule induces, by binding to hemoglobin, a decrease in the affinity of hemoglobin for oxygen, thereby leading to improved release of oxygen from hemoglobin in peripheral tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Reduced oxygen transport capacity as a cause of dyspnea]. 804 64

A 5-year-old girl was diagnosed as having idiopathic thrombocytopenic purpura (ITP) based on symptoms of nasal bleeding and purpura. The platelet count was 35,000/microliters without anemia or leukopenia. Micromegakaryocytes were observed in normocellular bone marrow without dyserythropoiesis or dysgranulopoiesis. She had periosteal fibroma of the rib and atopic dermatitis with elevated serum IgE. Prednisolone and azathioprine were administered but with no response. The cumulative dose of azathioprine was 20 g for 28 months. Nine years after the diagnosis of ITP, she was admitted because of dyspnea and anemia. The white cell count was 26,900/microliters with 17% monocytes. The hemoglobin was 3.9 g/dl and the platelet count was 9,000/microliters. Dyserythropoiesis, dysgranulopoiesis and micromegakaryocytes were observed in hypercellular bone marrow. The chromosome analysis demonstrated 47, XX, +21. She was diagnosed as having chronic myelomonocytic leukemia (CMMoL) and received bone marrow transplantation (BMT) from an HLA-identical sibling conditioned with high-dose busulfan and melphalan. After 17 months of remission, the disease recurred with an abnormal karyotype of 47, XX, +21, 7q+. Despite a second BMT conditioned with high-dose etoposide, cyclophosphamide and total body irradiation, she died of the disease. Refractory thrombocytopenia as a subgroup of myelodysplastic syndrome, rather than ITP, might have preceded the development of CMMoL, with the possibility of azathioprine-induced leukemia.
 ...
PMID:[Chronic myelomonocytic leukemia developed 9 years after the diagnosis of idiopathic thrombocytopenic purpura in a child]. 807 97

A total of 4676 patients and 1759 patients were treated with lisinopril and nifedipine respectively in a post-marketing surveillance study conducted in general practice in the UK. Patients were followed up for 12 months. Most of the lisinopril patients had hypertension, but a small number (180) had heart failure. Most of the nifedipine patients had uncomplicated hypertension, but some (22.57%) had other cardiovascular disease with or without hypertension. Lisinopril and nifedipine were equally effective in reducing blood pressure. During the study, 1.5% of hypertensive patients assigned to lisinopril died compared with 1.8% of patients assigned to nifedipine, and 15.1% of lisinopril patients compared with 19.7% of patients in the nifedipine group withdrew because of adverse events. Cough, malaise and fatigue, nausea and vomiting were more frequent causes of withdrawal from lisinopril than nifedipine. Conversely, headaches, pallor and flushing, oedema and palpitations caused more frequent withdrawals from nifedipine. Anaemia was more often encountered on nifedipine treatment than on lisinopril. In hypertensive patients, the frequency of first-dose hypotension was similar on both treatments. Serious events occurred in 0.8% and 0.5% of patients given lisinopril and nifedipine respectively. Lisinopril was well tolerated by heart failure patients: 16 patients (8.88%) died and an incidence of 4.44% of serious adverse events was reported, a pattern to be anticipated in such patients; dizziness, giddiness, dyspnoea, cough, nausea and vomiting were the most frequent causes of withdrawal; the incidence of first-dose hypotension was low (2.22%).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Post-marketing surveillance of lisinopril in general practice in the UK. 811 50

A 19-year-old man with acute lymphoblastic leukaemia developed fever, general deterioration and somnolence 3 days after a cycle of cytostatic treatment. He had anaemia (haemoglobin 6.6 g/dl), leukopenia (100/microliters) and thrombocytopenia (7,000/microliters). As an acute septicaemia was suspected he received broad spectrum antibiotic therapy, together with two units of red cell and platelet concentrates. However, his condition worsened rapidly over the next 5 hours (meningism, seizures, fever to 41.1 degrees C, dyspnoea). Another blood count revealed severe haemolysis. Computed tomography of the skull demonstrated multilocular intraparenchymal gas formation. Although the antibiotic treatment was extended the patient died several hours later. Retrospective examination for suspected transfusion mismatch provided no evidence for erythrocyte incompatibility. But there was liberation of T-antigen as sign of a bacterial cause of erythrocyte damage. An anaerobic blood culture grew Clostridium perfringens. This case demonstrates that acute intravascular haemolysis in septicaemia should be considered in the differential diagnosis of transfusion mismatch.
 ...
PMID:[Acute intravasal hemolysis in Clostridium perfringens sepsis. Differential diagnosis of hemolytic episodes]. 813 16


<< Previous 1 2 3 4 5 6 7 8 9 10