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)

Adriamycin has a wide spectrum of antitumor activity with dose related cardiotoxicity as a major side effect. The objective of this study was to investigate the influence of captopril, a sulphydryl containing angiotensin converting enzyme inhibitor, on the cardio- and hematotoxicity of adriamycin in normal rats. A single dose of adriamycin (15 mg/kg) caused myocardial toxicity after 24 h manifested biochemically by elevation of serum enzymes:- Aspartate transaminase (AST, EC: 2.6.1.1), lactate dehydrogenase (LDH, EC: 1.1.1.27), creatine phosphokinase (CPK, EC: 2.7.3.2) and the cardiac iso-enzymes of LDH and CPK. The hematotoxicity was characterized by severe leukopenia and anemia that appeared after 72 h of adriamycin administration. Captopril (60 mg/kg i.p.) 1 h before adriamycin injection ameliorated the biochemical toxicity induced by adriamycin. This was evidenced by a significant reduction in serum enzymes, after 24 and 48 h and a significant reduction of serum cardiac iso-enzymes after 48 h. Also restoration of the white blood cell counts as well as hemoglobin concentration occurred after 72 h of captopril administration. These results suggest that captopril may be benificial as a protective agent against cardio- and hematotoxicity induced by adriamycin.
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PMID:Captopril ameliorates myocardial and hematological toxicities induced by adriamycin. 967 64

An 80-year-old woman was admitted with anemia, jaundice and a bleeding tendency about 5 weeks after starting omeprazole. On admission, the hemoglobin was 6.4 g/dl, platelets 0.1 x 10(4)/microliter, leukocyte count 7,500/microliter, and reticulocyte count 325/1000. The total bilirubin was 1.9 mg/dl, indirect bilirubin 0.6 mg/dl, lactate dehydrogenase 572 IU/l, and haptoglobin < 10 mg/dl. Both the direct and the indirect Coombs' tests were positive. The platelet-associated IgG (PAIgG) was 1,100.0 ng/10(7) cells. A decrease in the complement value was observed. There was an increase in the number of megakaryocytes and erythroblasts in the marrow film. After omeprazole administration was halted, her hemoglobin and platelet levels gradually returned to normal. On the 27th hospital day, the direct Coombs' test was positive but the indirect Coombs' test became negative. The PAIgG value also returned to normal, and she was discharged on the 59th hospital day. The acute phase of the drug-induced lymphocyte stimulation test was negative, however, we detected the IgG antibody to omeprazole. In the recovery phase, the IgG value decreased. Forty days after discharge, the direct Coombs' test had become negative. This is apparently the first report of a patient with acute hemolytic anemia and thrombocytopenia due to omeprazole through an immune complex mechanism.
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PMID:[Hemolytic anemia and thrombocytopenia associated with anti-omeprazole antibody]. 969 74

We describe a 27-month-old boy who was first admitted to our hospital on 7 January 1995 with nasal bleeding. From 6 months of age he has had lymphadenopathy, low levels of serum uric acid, increased levels of serum lactate dehydrogenase and hyper gamma-globulinemia. From the age of 18 months he has had persistent Epstein-Barr virus (EBV) infection (target cells; B cells), recurrent episodes of thrombocytopenia, anemia and hepatosplenomegaly. Dysmobility of the left leg and arm from a central nervous system complication during a relapse with pancytopenia on March 1995, was also observed. Relapses of thrombocytopenia with increases of platelet-associated immunoglobulin G and hepatosplenomegaly have been observed approximately every 2 months, and two relapses of pancytopenia were accompanied with weak positivity of Coombs test and low level of haptoglobin. These recurrent episodes were improved with prednisolone. However, now in June 1997 we have not been able to diagnose what underlies the above clinical symptoms, except that the patient has a persistent EBV infection.
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PMID:Recurrent hepatosplenomegaly and peripheral blood cytopenia, persistent Epstein-Barr virus infection and central nervous system manifestation in a patient with lymphadenopathy and low serum uric acid. 974 82

A 72-year-old patient presented himself with typical symptoms of coronary heart disease and was scheduled for invasive diagnostic procedures. Cardiac risk factors were smoking and arterial hypertension. The physical examination was inconspicious. In the laborchemistry a hemoglobin of 79 g/l with a mean corpuscular volume of 63 fl and a mean corpuscular hemoglobin of 20 pg was conspicuous. The serum iron was with 42 micrograms/dl in the lower norm. Transferrin, bili-rubin and lactate dehydrogenase were normal. Then in the gastrointestinal investigations he was diagnosed with a leiomyoma of the intestine that led to chronic anaemia and additionally to chest pain characteristic for angina pectoris. After the removal of the tumor and normalization of hemoglobin this patient was free from symptoms of the disease. The coronary angiography revealed a complex stenosis of the right coronary artery with collaterales and not significant stenosis both of the left coronary arteries. In patients with angina pectoris anaemia as the possible and only cause of angina ought to be verified. It is therefore necessary after normalization of hemoglobin and clarification of the cause for the anaemia to apply a test for coronary ischemia.
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PMID:[Angina pectoris in leiomyoma]. 975 77

We describe the case of a 44-year-old woman with a delayed hemolytic transfusion reaction (DHTR). She had a history of two pregnancies and a blood transfusion, the details of which were unknown. At the time of her first vascular surgery on November 15, 1989, she received 1200 ml of crossmatch-compatible concentrated red blood cells (CRC). Before the first operation, screening for anti-RBC antibodies (Ab) was negative. At the time of the second admission on Feburary 15, 1996, anti-E Abs were detected by indirect antiglobulin test. She received 560 ml of E-antigen-negative, crossmatch-compatible, CRC for treatment of anemia on March 1 and 2, 1996. After this transfusion, total bilirubin (1.6 mg/dl) and lactate dehydrogenase (1355 IU/ml) were elevated on March 12, 1996. She had no evidence of clinical hemolysis. We suspected DHTR from these data, and therefore screened for anti-RBC Abs. Anti-E, Jka, Dia, Fyb, and S Abs were detected in blood samples obtained from the patient on March 12, 1996. Anti-E, Jka Dia, and S Abs were present more than 1 month and anti-Fyb Ab was disappeared at 18 days after transfusion.
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PMID:A delayed hemolytic transfusion reaction (DHTR) with multiple alloantibodies (Anti-E, Jka, Dia, Fyb, and S) induced by E-antigen-negative, crossmatch-compatible blood. 980 32

Disseminated Mycobacterium avium complex (DMAC) infection is a common complication of advanced HIV disease, and is an independent predictor of mortality. The clinical features of DMAC infection are fever, weight loss, abdominal pain, anemia, elevated serum alkaline phosphatase, and elevated serum lactate dehydrogenase. The diagnosis is made by blood cultures; clinical diagnosis is unreliable. Chemoprophylaxis of DMAC infection with azithromycin is recommended when the CD4 lymphocyte count is below 50 cells/mm3. Established DMAC infection is treated with clarithromycin plus ethambutol, unless the isolate is macrolide-resistant, in which case the optimal therapy is uncertain. Highly active antiretroviral therapy is important in both prevention and treatment of DMAC infection.
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PMID:Prevention and treatment of disseminated Mycobacterium avium complex infection in human immunodeficiency virus-infected individuals. 983 75

We analyzed 33 patients with AILD T-NHL in a retrospective multicentric study. The median age was 62 yr (35-84 yr) (19 patients over 60 yr). Advanced disease (n = 31) and B-symptoms were consistently found (n = 29) and 20 patients had bone marrow involvement. The main laboratory abnormalities were: anemia (n = 13), hypereosinophilia (n = 13), lymphopenia (n = 14), hypergammaglobulinemia (n = 17), elevated lactate dehydrogenase (LDH) level (n = 24). First-line therapy was chemotherapy (ChT) alone (n = 25) or ChT after steroids (n = 8). Most patients received a CHOP-like regimen for a median number of 6 cycles and 3 patients received interferon alpha (IFN alpha) as consolidation after chemotherapy. With a median follow-up of 46 mo, 60% achieved a complete response but the outcome was poor with a relapse rate at 56%, a median survival referring to the total population was of 36 mo (2-108+ mo) and an overall survival at 5 yr of 36%. Two patients received high-dose chemotherapy (with total body irradiation) and autologous progenitor-cell transplantation for chemosensitive relapse and were free of disease at, respectively, 76 and 24 mo+. In conclusion AILD T-NHL still has a poor prognosis compared to other NHL. The role of intensive therapy and IFN alpha still remains to be evaluated.
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PMID:Angioimmunoblastic-like T-cell non Hodgkin's lymphoma: outcome after chemotherapy in 33 patients and review of the literature. 1004 27

There is a large variability in the severity of the clinical manifestations of sickle cell anemia (SSA), including renal involvement. Haplotypes in the beta-globin gene cluster associated with the geographical origin of the sickle mutation, as well as microdeletions in the alpha-globin genes, could provide an epigenetic influence on the heterogeneous outcome in SSA. It has been determined that the cause of progressive renal insufficiency in SSA is a glomerulopathy, clinically detected by the presence of macroalbuminuria (albumin excretion rate >300 mg/g creatinine). To investigate the role of the alpha-globin gene microdeletion and beta-globin gene cluster haplotypes on the degree of glomerular involvement, 76 adult SSA patients (hemoglobin SS) were studied to determine the relationship between these genetic markers and the development of sickle cell glomerulopathy. Macroalbuminuria was present in 22 (29%) of 76 adult SSA patients. The coinheritance of microdeletions in one or two of the four alpha-globin genes (alpha-thalassemia) was associated with a lower prevalence of macroalbuminuria (13%) versus patients with intact alpha-globin genes (40%, P = 0.01). By contrast, there was no association between albuminuria and beta-globin gene haplotypes (Central African Republic [CAR] versus non-CAR haplotypes). Patients with alpha-globin gene microdeletions had lower mean corpuscular volumes and mean corpuscular hemoglobin concentration than patients with all four alpha genes (86+/-2 versus 99+/-3 fl, and 33.9+/-0.2 versus 34.9+/-0.2%, respectively, P<0.05). There were no such hematologic differences between CAR and non-CAR beta-globin haplotypes. There were no differences in duration of disease (age), hemoglobin levels, reticulocyte index, and lactate dehydrogenase levels between those with and without glomerulopathy, but the mean arterial pressure was higher (87+/-1 mm Hg) in patients with intact alpha gene locus versus those with microdeletions (80+/-2 mm Hg, P<0.05). It is concluded that the coinheritance of microdeletions in the alpha-globin gene locus in SSA patients confers "renoprotection" by mechanisms not related to the degree of anemia or the severity of hemolysis, but could be related to a reduced mean corpuscular volume or to a lower erythrocyte hemoglobin concentration.
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PMID:Evidence that microdeletions in the alpha globin gene protect against the development of sickle cell glomerulopathy in humans. 1023 87

The authors present the characteristics of a group of 23 patients with mantle cell lymphoma. In the group only a slight predominance of men over women was found (1.1:1), the median age was 63 years. Twenty-one (91%) of the patients were diagnosed in stage IV (Ann Arbor). In all these patients the bone marrow was affected. In 19 of them immunoflowcytometric analysis revealed the typical clone of B lymphocytes (CD5 positive)/CD 23 negative). The majority of patients had at the time of diagnosis a large tumourous mass with massive splenomegaly (61%), hepatomegaly (57%) and bulky disease (52%). The node was excised in 17 patients, but in four patients (24%) during the first session the diagnosis was not assessed correctly. In the laboratory findings an inclination to anaemia, thrombocytopenia, lymphocytosis and in particular to high levels of serological indicators of activity of the disease dominated--lactate dehydrogenase, beta-2-microglobulin and serum thymidine kinase. All patients were treated by chemotherapy. Complete remission was achieved by the date of evaluation in one patient (4%), partial remission in seven patients (30%) but 48% patients did not respond to first line treatment. Nine patients of the group died, their median of survival was 14 months (0-24), the median of the follow up of the remaining patients was 133 months (2-31). Two female patients had large-dose treatment with subsequent administration of autologous stem cells. The first one is after 370 days of treatment in complete remission, the second one developed a relapse 100 days after the procedure. From the results and analysis of the literature ensues that mantle cell lymphoma is one of the aggressive malignant B-lymphoproliferations with a very adverse prognosis and it deserves therefore special diagnostic and intense therapeutic attention.
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PMID:[Mantle cell lymphoma as a diagnostic and therapeutic problem]. 1042 28

Excess morbidity and mortality among long-term hemodialysis patients because of infectious complications is partly caused by an impairment of cellular immune defense. We hypothesized this impairment is related to an abnormal carnitine metabolism also present in these patients. In a double-blind, randomized, placebo-controlled trial, we investigated the effect of L-carnitine on phagocytic function and viability of blood leukocytes in 17 patients undergoing maintenance hemodialysis. After an observation period of 1 month, the patients received either 10 mg/kg of L-carnitine or placebo intravenously at the end of each hemodialysis session over a period of 4 months. Leukocyte oxidative metabolism was measured by means of luminol-enhanced chemiluminescence and superoxide generation after stimulation with Staphylococcus aureus or phorbol myristate acetate. Killing capacity and phagocytosis of radiolabeled staphylococci were determined. A lactate dehydrogenase (LDH) release test was applied to assess cell viability. We were unable to show an effect of L-carnitine on phagocytic function and viability in vivo. Several clinical parameters were observed during the trial. No statistically significant differences concerning dialysis-related morbidity, anemia, or reduction of blood urea nitrogen and creatinine levels were detected. Additionally, we tested the effect of L-carnitine on phagocytic function after in vitro incubation of blood leukocytes, which also showed no changes. LDH release was decreased, indicating an improved viability of these cells. The latter results were found after in vitro incubation of cells, but could not be confirmed in vivo. In summary, we could not show beneficial effects of L-carnitine administration in hemodialysis patients for the dosage and duration of treatment stated, either on phagocytic function and viability or on the clinical and biochemical parameters observed.
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PMID:Effects of L-carnitine on leukocyte function and viability in hemodialysis patients: A double-blind randomized trial. 1051 49


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