Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After an outbreak of hepatitis B virus (HBV) infection in a unit of pediatric oncology, the clinical outcome and HBV markers were followed in 1 child with chronic and 10 children with acute HBV infection for 12 months. Four children had acute hepatitis with jaundice whereas 7 of the infections were subclinical. Ten children had antecedent malignancies and 1 had aplastic anemia. Four patients died of causes unrelated to the hepatitis after periods of 2, 4, 8 and 10 months. All 3 children who were not immunosuppressed at the time of contracting the HBV infection quickly turned negative for hepatitis B surface antigen (HBsAg), whereas only 2 of 8 patients who were immunosuppressed by chemotherapy eventually became HBsAg-negative. The latter 8 patients were also hepatitis B e antigen (HBeAg)-positive. Two of them quickly cleared HBeAg, but 6 remained HBeAg-positive throughout the follow-up. In 6 of 9 patients HBsAg was also detected in saliva. These results suggest that children who are receiving anticancer chemotherapy have an increased risk of remaining HBeAg-positive and secreting HBsAg and possibly HBV in their saliva, which makes them particularly infective.
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PMID:Characteristics and outcome of acute infection with hepatitis B virus in children with cancer. 834 11

Paroxysmal nocturnal haemoglobinuria (PNH) is now generally accepted as a disease in which bone marrow derived cells are deficient in phosphatidylinositolglycan (PIG)-anchored surface molecules. A series of new monoclonal antibodies detecting PIG-anchored surface structures on human leucocytes (CD48, CD55, CD59) has recently been described. In the present study 12 patients with the diagnosis PNH and a positive Ham test were examined for PIG-anchored surface antigen expression on various cell lineages using immunofluorescence. In all patients deficient cells were detected in erythrocyte, granulocyte and monocyte analysis. A deficient lymphocyte subset was also observed in all but one of these patients. Using two-colour analysis, all lymphocyte subpopulations such as T, B and NK cells were found to be affected. In addition, peripheral blood cells of 22 patients with severe aplastic anaemia (SAA) were tested for the PIG-anchoring defect. In five of these patients the defect was detected, and in four of the five the lack of PIG-anchored molecules was confined to the granulocyte and monocyte lineages apparently without affecting the erythrocytes. The results of these studies demonstrate that cytofluorographic testing of peripheral blood cells provides a simple and reliable method for establishing the diagnosis of PNH. Furthermore, especially in the case of aplastic anaemia patients, the sensitivity of immunophenotyping might be superior to conventional laboratory tests.
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PMID:Diagnosis of paroxysmal nocturnal haemoglobinuria using immunophenotyping of peripheral blood cells. 175 77

Among 262 inpatients with hematologic diseases who were referred for chemotherapy or immunosuppressive therapy between January, 1985, and December, 1989, nine (3.4%) patients, including two with Hodgkin's disease (HD), three with acute myeloblastic leukemia, one with chronic myelogenous leukemia, two with multiple myeloma and one with aplastic anemia, were found to be hepatitis B virus (HBV) carriers before their chemotherapy began. All six HBV carriers who received chemotherapy containing glucocorticoid showed mild-to-moderate elevations in serum transaminase levels after the chemotherapy. Five showed a rise in titer of the hepatitis B surface antigen, HBsAg. In contrast, three HBV carriers not receiving glucocorticoid showed no change in serum transaminase after chemotherapy. One HBV carrier with HD suffered from severe icteric hepatitis after the withdrawal of multiagent chemotherapy containing glucocorticoid. The HBV-DNA polymerase rose markedly and was accompanied by a marked rise in titer of HBsAg. The results warn us to keep in mind the possibility of glucocorticoid inducing an activation of HBV infection, which may result in severe hepatitis in some HBV carriers. Although further investigation is required, it is recommended that HBsAg-positive patients with hematologic malignancies should, if possible, be treated without glucocorticoid.
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PMID:Activation of hepatitis B virus infection by chemotherapy containing glucocorticoid in hepatitis B virus carriers with hematologic malignancies. 175 16

Among 145 consecutive patients undergoing bone marrow transplantation (BMT) for leukemia or aplastic anemia. 30 (21%) were found positive for hepatitis B surface antigen (HBsAg) in serum either before or after BMT. Their serologic profile and clinical outcome are described. Nine out of 30 patients were HBsAg positive before BMT: four were chronic carriers and five were found HBsAg+ at transplant. Three of the former and one of the five latter patients remained persistently HBsAg+ after transplant with signs of liver disease; none developed liver failure, indicating that HBsAg positivity is not an absolute contra-indication to BMT. Among the remaining 21 patients. HBsAg was detected early (n = 12) or late (n = 9) after transplant. All 21 cleared the antigen during follow-up and liver disease was either mild and asymptomatic (nine cases) or clinically overt (12 cases), but none had life-threatening liver disease. Several HBV-infected patients were constantly seronegative for antibody to HBcAg even in the presence of active HBV replication. These results show that the serologic pattern of HBV markers in BMT patients is unpredictable. HBV infection was rarely associated with severe hepatitis and HBsAg carriage.
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PMID:Hepatitis B virus (HBV) infection and liver disease after allogeneic bone marrow transplantation: a report of 30 cases. 239 Jun 30

Ninety patients with a strict diagnosis of aplastic anemia were observed during a 4-year period. The incidence of aplastic anemia is estimated to be much higher here than in western countries. A disproportionately large number of young males were noted among our patients. Two cases were congenital. One case presented a past history of paroxysmal nocturnal hemoglobinuria. The etiology of 8 cases (8.9%) could be attributed to drugs and/or chemicals. In the remaining 79 cases (87.8%), the causes of the disease were unknown. The carrier rate of the hepatitis B surface antigen in the patients with aplastic anemia was similar to that of the general population, and chronic hepatitis B infection was not considered a major etiological factor. Coexistence of abnormal liver functions at the initial presentation was noted in 21.9% of the patients. Exposure to unknown drugs by self-medication was possibly one of the major causes of the high incidence of aplastic anemia and the associated abnormal liver functions in our patients.
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PMID:Aplastic anemia in Taiwan and its etiological factors. 263 49

Severe aplastic anemia is a rare but important complication of hepatitis. The agent(s) responsible for the hepatitis in these cases have not been well defined. Sixteen patient with hepatitis-associated aplastic anemia were studied for evidence of recent infection with hepatitis A virus, hepatitis B virus, cytomegalovirus, Epstein-Barr virus, and Toxoplasma. Results were compared with data from 10 randomly selected patients with aplastic anemia unassociated with hepatitis. Of the 16 patients, recent acute hepatitis A infection could be excluded in at least 14 patients. Hepatitis B surface antigen (HBsAg) was present in only one patient. A diagnosis of recent hepatitis B infection could not be excluded with confidence in two others. Tests for cytomegalovirus, Epstein-Barr virus, and Toxoplasma gave negative results. No patient with aplasia unassociated with hepatitis had evidence of recent hepatitis A infection, and the frequency of hepatitis B antibodies in this group was indistinguishable from that in patients with hepatitis. These data indicate that most cases of hepatitis that preceded aplastic anemia were not caused by hepatitis A virus or hepatitis B virus; non-A, non-B agents were probably involved in at least 13 of the 16 cases studied.
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PMID:Aplastic anemia and non-A, non-B hepatitis. 629 45

Chronic exposure of humans to benzene (BZ) affects hematopoietic progenitor cells in intermediate stages of differentiation which can lead to aplastic anemia and/or acute myelogenous leukemia and some of its variant forms. We studied the effects of BZ and hydroquinone (HQ), a toxic bone marrow metabolite, on the human HL-60 promyelocytic leukemic cell line. Because the HL-60 cell is bipotential and can be induced to differentiate to monocytes or granulocytes it has been used in many studies as a surrogate for the granulocyte/macrophage committed cell, GM-CFU. Treatment of HL-60 cells with BZ specifically induced differentiation along the granulocytic lineage as measured by morphology, induction of superoxide production and chloroacetate esterase activity and the appearance of the L12-2 surface antigen. Differentiation was induced via the activation of protein kinase C and the phosphorylation of several proteins known to be involved in HL-60 cell differentiation. Subsequent to kinase C activation, arachidonic acid was released from membrane phospholipids and the 5-lipoxygenase pathway was activated for the production of leukotriene D4 (LTD4) required for granulocytic differentiation. BZ induction of granulopoiesis was prevented by preincubation of HL-60 cells with inhibitors of protein kinase C, 5-lipoxygenase, gamma-glutamyl transpeptidase required for the conversion of LTC4 to LTD4, or LTD4 receptor antagonists. Treatment of HL-60 cells with tetraphorbol myristate acetate (TPA), 1 alpha, 25-dihydroxyvitamin D3 (1,25-(OH2)D3) or interleukin-1 (IL-1) induced HL-60 cells to differentiate to monocytes/macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of benzene and hydroquinone on myeloid differentiation of HL-60 promyelocytic leukemia cells. 812 4

We report herein the case of a 35-year-old woman with aplastic anemia who developed hepatocellular carcinoma after long-term therapy with oxymetholone. She was treated with 60 mg/day of oxymetholone for 3 years (total dose 64.8 g). Alpha-fetoprotein, hepatitis B surface antigen, and hepatitis C antibody were all negative, but serum titers of carcinoembryonic antigen and carbohydrate antigen were elevated. Lateral segmentectomy of the liver was performed. The histopathological findings were compatible with those of multiple hepatocellular carcinoma without liver cirrhosis. Three years since the operation, the patient is doing well and no signs of tumor recurrence have been detected. According to our review of Japanese cases of hepatocellular carcinoma associated with anabolic steroid therapy, in all instances the tumors developed after long-term administration of anabolic steroids for hematologic diseases. In patients under long-term anabolic steroid therapy, routine screening of the liver by ultrasonography and computed tomography should be performed to detect liver tumors in the early stages.
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PMID:Hepatocellular carcinoma associated with anabolic steroid therapy: report of a case and review of the Japanese literature. 872 41

Between 1971 and 1989 we have treated 19 patients with hepatitis-associated aplastic anemia by marrow transplantation from their HLA-identical siblings following conditioning with 200 mg/kg cyclophosphamide (Cy) administered over a period of 4 days. One patient failed to engraft by day 34 and was given a second transplantation. He died from infection 15 days after the second transplantation. Eighteen patients had sustained engraftment. Six patients developed acute graft-vs.-host disease (GVHD) and two of these patients died 2.8 and 3.3 months after transplantation. Fifteen patients are surviving 4 to 24 (median 13) years after transplantation, while one patient died in a car accident 17 years after successful transplantation. Six of the surviving patients developed chronic GVHD. Two of the patients with chronic GVHD had preceding acute GVHD and four did not. Five of the six patients with chronic GVHD received donor buffy coat cells in addition to the marrow inoculum to prevent graft rejection. Twelve of the 15 surviving patients have Karnofsky performance scores of 100%. One patient, living more than 4 years after transplantation, has a Karnofsky score of 40% because of persistent cognitive deficits following non-A, non-B hepatitis with hepatic coma. Two patients developed hepatitis C infection 12 and 18 years after transplantation, respectively. Except for mild fatigue and mildly elevated liver function tests, these patients are doing well with Karnofsky performance scores between 95 and 100%. One patient developed severe coronary artery disease 10 years after transplantation, decreasing his Karnofsky performance score to 80%. Serum samples before and after transplantation from 13 patients were tested for hepatitis B virus (HBV) DNA and hepatitis C virus (HCV) RNA by polymerase chain reaction (PCR). Only one patient tested positive for HCV RNA before transplantation. Seven of 15 sera were hepatitis C RNA-positive posttransplantation, but only one of these patients has developed active hepatitis C. All 13 patients were were negative for hepatitis B surface antigen and HBV DNA. Only one patient had IgM antibodies against hepatitis A virus (HAV) before transplantation, which suggested HAV infection. Hepatitis-associated aplastic anemia apparently was caused in most patients by a non-A, non-B, non-C agent. HLA-identical marrow transplantation for hepatitis-associated aplastic anemia with Cy as conditioning regimen is well-tolerated and has a long-term event-free survival in excess of 80%, not different from results of marrow transplantations for aplastic anemia of other etiologies.
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PMID:Marrow transplantation for hepatitis-associated aplastic anemia: a follow-up of long-term survivors. 911 4

Aplastic anemia is more common in the Orient than in western countries, with an incidence in Thailand that is 2- to 3-fold higher than in Europe. Aplastic anemia after hepatitis is a well characterized clinical entity, and clinical hepatitis is also prevalent in the Far East. We performed a prospective case-control study to determine risk factors for aplastic anemia in Bangkok and two rural regions during 1989 to 1994. A total of 375 cases were identified, along with 1,174 hospital controls matched for age and sex. Historical data were collected by trained interviewers. Sera from a subset of cases (N = 177) and controls (N = 183) were tested for antibodies to hepatitis viruses A, B, and C and hepatitis B surface antigen. There was no evidence of association of aplastic anemia with hepatitis B or hepatitis C. Previous exposure to hepatitis A, as determined by immunoglobulin G (IgG) seropositivity, was significantly associated with aplastic anemia: the relative risk adjusted for confounding was 2.9 (95% confidence interval 1.2-6.7). The same association also existed for persons under age 25 years, in whom the prevalence of hepatitis A IgG was lower than in the total population. However, no patients showed evidence of recent infection with hepatitis A (immunoglobulin M [IgM] seropositivity). These results indicate that exposure to a hepatitis virus is a risk indicator for aplastic anemia in Thailand, and while itself unlikely to be etiologic, hepatitis A may be a surrogate marker for another enteric microbial agent.
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PMID:Association of seropositivity for hepatitis viruses and aplastic anemia in Thailand. 939 21


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