Search PubMed⌕ Search

Biomedical subjects

F Bauters

Publications and source records attributed to F Bauters.

At least 109 records · Page 6Linked to original sources
PubMed1993

Cerebrospinal fluid neopterin levels in children with central nervous system leukemia.

Cerebrospinal fluid (CSF) neopterin levels were determined by high-pressure liquid chromatography in 48 normal children and in 15 children with meningeal relapse of hematologic malignancies (13 acute lymphoblastic leukemia and 2 high-grade lymphomas). When meningeal relapse was diagnosed, all patients had CSF neopterin levels higher than mean normal value +2 standard deviations. No significant correlation between the blast count in the CSF and neopterin levels was observed. CSF data before relapse were available in 10 children: the neopterin values at relapse were significantly higher than values observed at diagnosis. In 3 patients, elevated neopterin levels preceded the occurrence of neurologic signs and the detection of blast cells in CSF by 15 to 30 days. In the absence of infection, the rise of CSF neopterin levels in patients with hematologic malignancies indicates an active phase of the disease. This could reflect a cell-mediated immunologic process induced by malignant cells. The measurement of CSF neopterin should be helpful in the monitoring of patients to detect early meningeal relapse.

Adolescent↗
PubMed1993

Cytogenetic analysis has strong independent prognostic value in de novo myelodysplastic syndromes and can be incorporated in a new scoring system: a report on 408 cases.

Although the prognostic value of cytogenetic analysis has previously been demonstrated in myelodysplastic syndromes (MDS), karyotype had not been included in previously published scoring systems, such as Bournemouth and Sanz's scores. We studied karyotype at diagnosis in 408 cases of de novo MDS (after excluding therapy-related MDS). Karyotypes were classified in 10 groups: normal; isolated del 5q; del 5q and other rearrangements; isolated +8; isolated -7 or del 7q; del 20q; isolated -Y; miscellaneous single rearrangements; -7 or del 7q and other rearrangements; miscellaneous complex rearrangements. Karyotypes were considered complex when at least three chromosomes were rearranged. Complex karyotypes included all patients with del 5q and other rearrangements, -7 or del 7q and other rearrangements, and miscellaneous complex rearrangements (i.e. three of the 10 groups). Median actuarial survival of the 408 patients was 28 months, and 90 patients (22%) progressed to acute myeloid leukemia (AML). For survival, bone marrow (BM) blasts, circulating blasts, white blood cell (WBC), neutrophil count, platelet count, hemoglobin, age, sex, FAB classification, and Bournemouth and Sanz's scores had strong prognostic value. Cytogenetics also had strong prognostic value. An unfavorable cytogenetic group (patients with complex karyotypes) was identified. On the other hand, although patients with isolated del 20q and del 5q had a somewhat better prognosis than other patients with non-complex cytogenetic findings, they could not be statistically individualized as a favorable group, possibly owing to their relatively limited number. By multivariate regression analysis, a three-variable new scoring system could be designed based on karyotype (1 point for complex karyotype; 0 for other groups), platelets (0 for > 75 x 10(9)/l; 1 for < 75 x 10(9)/l), and BM blasts (0 for < 5%, 1 for 5-10%, 2 for > 10%). The total score (addition of points for the three variables) was able to separate patients in three groups with low (score 0) intermediate (score 1 or 2), and high risk (score 3 or 4) which included 34%, 47%, and 19% of the patients, and had a median survival of 55, 24, and 6 months, respectively (chi 2 = 110, p < 10(-4)). This new score (Lille score) was able to subdivide risk groups according to Bournemouth and Sanz's scores into further subgroups of different prognoses. For progression to AML, BM blasts, circulating blasts, WBC count, hemoglobin, FAB type, and karyotype had prognostic value by univariate analysis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1993

[Acute necrotic pancreatitis secondary to asparaginase. Role of drug combinations--early diagnosis and treatment. Apropos of 2 cases].

Acute necrotic pancreatitis was diagnosed in two patients treated with asparaginase for, in the first case a highly malignant lymphoma and in the second an acute lymphoblastic leukemia. The diagnosis on clinical findings and amylase assay results was confirmed by LDH and/or C reactive protein values and abdominal CT scans. Both patients recovered after drainage of peripancreatic fluid collections, in the first patient by surgical followed by cutaneous drainage and in the second by cutaneous drainage of a pancreatic pseudocyst. In addition to the frequent pancreatic reaction observed during asparaginase treatment, signs of pancreatic necrosis requiring urgent treatment have to be identified. The necrotic nature of the pancreatitis was confirmed by clinical examination, assay to biologic markers and abdominal CT scans, eliminating other causes of the pancreatitis.

Acute Disease↗
PubMed1992

Accessory spleen in recurrent chronic immune thrombocytopenic purpura.

From 1969 to 1985 we discovered accessory spleens in 8 patients with chronic immune thrombocytopenic purpura (ITP) who relapsed or failed after splenectomy. Imaging of accessory spleen used a liver spleen scintigraphy with heat-treated RBC labeled with Tc-99m. Platelet kinetic studies with 51Cr or 111In, including sequestration index, were performed. Five patients had accessory splenectomy. Disappearance of bleeding symptoms was achieved in the 5 splenectomized patients but with only partial response of platelet counts. These results are discussed in the context of diagnosis and therapeutic management of accessory spleens in patients with chronic immune thrombocytopenic purpura who relapsed or failed after splenectomy.

Adolescent↗
PubMed1992

Secondary acute lymphoblastic leukemia with t (4;11): report on two cases and review of the literature.

We report two cases of secondary acute lymphoblastic leukemia (ALL) with t (4;11) (q21;q23) translocation occurring after chemotherapy and radiotherapy for a prior cancer. Seven previously published cases of secondary ALL with t (4;11) (q21;q23) are also reviewed. Most patients had received a combination of topoisomerase II inhibitors (anthracyclines, mitoxantrone, or the epipodophillotoxin derivatives VP16 or VM26) and cyclophosphamide, which have also been implicated in the pathogenesis of secondary acute myeloid leukemia (AML) with 11q23 rearrangements. These observations give further support to the existence of a subgroup of secondary acute leukemias with cytogenetic findings "specific" for de novo ALL and AML, especially those with translocations involving the 11q23 region.

Antigens, Differentiation↗
PubMed1992

Impairment of cerebral biogenic amine synthesis in a patient receiving high-dose methotrexate.

A transient acute neurologic syndrome occurred in a 15-year-old boy receiving high-dose methotrexate (MTX) for acute lymphoblastic leukemia. Cerebrospinal fluid analysis revealed a decrease of homovanillic acid and 5-hydroxyindoleacetic acid concentrations with a rise of biopterin levels. These findings suggest that MTX can induce a transient alteration of the metabolism of tetrahydrobiopterin leading to the defect of biogenic amine neurotransmitter synthesis.

Adolescent↗
PubMed1992

Acquired type II von Willebrand's disease associated with adrenal cortical carcinoma.

A case of acquired von Willebrand's disease (AvWD) associated with an adrenal cortical carcinoma is reported. The circulating highest molecular weight multimers (HMWM) of von Willebrand factor (vWF) were decreased when assessed by SDS-agarose plasma electrophoresis, leading to the diagnosis of type II AvWD. No forms of inhibitor could be detected in the plasma of the patient. In contrast, indirect immunoperoxidase studies with a monoclonal antibody to vWF demonstrated an absorption of vWF into malignant cells. Infusion of a vWF-FVIII concentrate, containing significant amounts of HMWM of vWF, allowed surgical resection of the tumour. After the first infusion of the concentrate, the vWF-RCo recovery was found to be low (38%) compared to the vWF:Ag (75%) and FVIII:C (163%) recoveries. The resolution of all biological signs of vWD, including the abnormal multimeric pattern, in the post-operative period was prompt and permanent. Therefore, the absorption of the HMWM of vWF by carcinomatous cells appears to represent a likely pathophysiological mechanism responsible for the AvWD syndrome in this patient.

Adrenal Gland Neoplasms↗
PubMed1992

Mutations of the P53 gene in acute myeloid leukaemia.

In a previous report we found point mutations in exons 5-8 of the P53 gene in five of 46 patients with acute myeloid leukaemia (AML), with a predominance of mutations in the 10 patients with 17p monosomy. In this report we extended our findings studying such mutations in 66 unselected additional cases of AML, using polymerase chain reaction single strand conformation polymorphism (SSCP) analysis and nucleotide sequencing. Three of the 66 new cases had a point mutation, leading to a change in one encoded amino acid. Thus, eight of the 112 AML studied had P53 mutations in exons 5-8, suggesting that the incidence of P53 mutation is relatively low in AML. A predominance of mutations in exon 8 (5/8) was found. Six of the eight patients with mutations were older than 60 years of age, and all eight cases had a short survival. All seven mutated cases karyotyped showed complex cytogenetic findings, especially monosomy 5 and/or 7, thus questioning the pathogenic importance of P53 mutations in a context of multiple genetic abnormalities. However, five of them also had 17p monosomy, and in the remaining two cases SSCP and sequence analysis also suggested loss of the normal P53 allele. This supported a role for the P53 gene mutations in leukaemogenesis in the relatively small number of AML patients in whom they were found, through loss of tumour suppressive activity of both normal P53 alleles, as reported in solid tumours.

Acute Disease↗
PubMed1992

Prognosis and treatment of lymphoblastic lymphoma in adults: a report on 80 patients.

PURPOSE: We analyzed prognostic factors in 80 adult patients with lymphoblastic lymphoma (LBL). PATIENTS AND METHODS: Twenty-one patients received six monthly courses of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) and maintenance chemotherapy for 12 months. The LNH-84 protocol (30 patients) consisted of four courses of high-dose CHOP followed by consolidation for 4 months. Both FRALLE (22 patients) and LALA (seven patients) protocols were two intensive chemotherapy regimens for acute lymphoblastic leukemia (ALL) that included an induction with daunorubicin, vincristine, cyclophosphamide, prednisolone (and asparaginase for the FRALLE regimen), consolidation, and maintenance chemotherapy that lasted for 2 years. RESULTS: Sixty-six patients (82%) achieved a complete remission (CR). The CR duration rate and overall survival rate at 30 months were estimated to be 46% and 51%, respectively, with a median follow-up of 55 months. Only two of 37 relapses occurred after 26 months. Chemotherapy protocol did not influence CR rate, CR duration, and survival. A higher CR rate was associated with an age of less than 40 years, lactic dehydrogenase (LDH) level of less than two times the upper limits of normal, and no or one extranodal site of disease. Short survival was associated with a failure to achieve CR, age older than 40 years, B symptoms, LDH level more than two times the upper limits of normal, and hemoglobin level of less than 100 g/L. Bone marrow involvement had no prognostic value. We could not evaluate precisely the prognostic value of Ann Arbor stage because inclusion criteria differed among treatment groups. CONCLUSION: Our findings suggest that age and LDH are two important pretreatment prognostic factors for adult LBL, and that the optimal prognostic staging system remains a controversial issue.

Adolescent↗
PubMed1992

Therapy-related acute promyelocytic leukemia: a report on 16 cases.

PURPOSE: To analyze the type of prior tumor and treatment in therapy-related acute promyelocytic leukemia (tAPL) that occurs after chemotherapy and/or radiotherapy (RT), and the hematologic characteristics and outcome of tAPL. PATIENTS AND METHODS: Sixteen patients with tAPL who were gathered during a 10-year period (1982 to 1991) in seven hematologic centers were analyzed retrospectively. RESULTS: There were 13 women and three men. The median age was 46 years (range, 12 to 82). Prior tumor was breast carcinoma in 10 cases, another solid tumor in three cases, and lymphoma in three cases. Two patients had received RT alone, and 14 had received chemotherapy (with RT in 11 cases). Prior chemotherapeutic agents generally included a combination of cyclophosphamide (used for limited periods), fluorouracil (5-FU), vinca alkaloids, and doxorubicin, mitoxantrone, or etoposide (VP16). By contrast, alkylating agents other than cyclophosphamide had been used in only two patients. Median interval between onset of treatment for the prior tumor and diagnosis of APL was 25 months. No patient had a known preleukemic phase. Hematologic and cytogenetic characteristics of the cases of tAPL were identical to those of the usual de novo APL, which included the presence of t(15; 17) in nine of the 10 patients tested. Two patients had early death. Seven patients were treated with intensive chemotherapy, and six achieved complete remission (CR). Three of them subsequently relapsed. Seven patients were treated with all-trans-retinoic acid (ATRA), and four achieved CR through the differentiation of blasts into mature granulocytes. None has relapsed so far. CONCLUSIONS: Our findings suggest that tAPL is not exceptional, and usually has several features in common with other types of therapy-related AML with specific karyotype (ie, t(8;21),t(9;11), inv(16)): solid tumor rather than hematologic malignancy as primary tumor, short interval of development, absence of known preleukemic phase, prior chemotherapy with a combination of several drugs that often included an agent that targets topoisomerase II (doxorubicin or mitoxantrone, but less often VP16). Hematologic characteristics and response to therapy (intensive chemotherapy or ATRA) in tAPL do not seem to differ from those of de novo APL.

Adolescent↗
PubMed1992

Mutations of the p53 gene in B-cell chronic lymphocytic leukemia: a report on 39 cases with cytogenetic analysis.

Mutations of exons 5 to 8 of the p53 gene were looked for in 39 cases of B-cell chronic lymphocytic leukemia (CLL) using polymerase chain reaction single-strand conformation polymorphism analysis and DNA sequencing. All patients also had cytogenetic analysis. A point mutation, leading to an amino acid change in the p53 protein was found in four cases, involving exon 7 (one case) or exon 8 (three cases). Mutations seemed to predominate in advanced clinical stages (Binet's stage C). All four patients with 17p monosomy had a mutation whereas no mutation was found in the 35 patients with cytogenetically normal 17p. These findings suggest that p53 mutations are relatively rare in B-cell CLL, and largely predominate or may even be restricted to patients with 17p monosomy (who constitute about 5% of all B-cell CLL patients in large published series). In those patients, the mutations may play a role in leukemogenesis through loss of tumor suppressive activity of normal p53 genes.

Aged↗
PubMed1992

Mutations of the p53 gene in B-cell lymphoblastic acute leukemia: a report on 60 cases.

Exons 5 to 8 of the p53 gene were examined for mutations in 60 patients with B-cell acute lymphoblastic leukemia (ALL), including 50 cases of precursor-B-cell ALL, nine cases of Burkitt (L3) ALL and one case of atypical ALL with surface immunoglobulins and t(8:14) translocation but L2 morphology. Karyotype was available in all patients. DNA was analyzed by polymerase chain reaction, single strand conformation polymorphism analysis, and nucleotide sequencing. Three patients showed point mutations in exons 7 or 8, including two of the nine patients with Burkitt ALL and one of the 50 patients with precursor-B-cell ALL. These findings suggest that p53 gene mutations are rare in precursor-B-cell ALL but may be more frequent in Burkitt ALL. In the three patients with p53 mutations, however, the relevance of those mutations to the development or progression of leukemia remained uncertain.

Amino Acid Sequence↗
PubMed1991

P53 gene mutations in acute myeloid leukemia with 17p monosomy.

We looked for mutations of exons 5 to 8 of the P53 gene in 10 patients with acute myeloid leukemia (AML) and 17p monosomy, and 36 patients with AML and no cytogenetic abnormalities of 17p. DNA was analyzed by polymerase chain reaction, single-strand conformation polymorphism analysis, and nucleotide sequencing. Four of the 10 patients with 17p monosomy showed point mutation, single-nucleotide deletion, or insertion in exons 7 or 8. By contrast, only 1 of the 36 patients with AML and no cytogenetic abnormalities of 17p showed a mutation of the P53 gene in exons 5 to 8 (P less than .01). These results suggest that alterations of the P53 gene may have a role in leukemogenesis in some cases of AML. The fact that P53 gene mutations occurred more often in patients with 17p monosomy seems to support the "recessive" model of tumor suppressive activity of the P53 gene rather than the "dominant" model, in which alteration of only one allele is sufficient for the development of malignancy.

Base Sequence↗
PubMed1991

Usefulness of electron microscopy in the diagnosis of congenital dyserythropoietic anemia type I: report of a case.

This report describes a case of congenital dyserythropoietic anemia (CDA) type I diagnosed in a 22-year-old woman with a two year history of macrocytic anemia. Light microscopy study of bone marrow disclosed only minor and nonspecific findings, without erythroid hyperplasia. Electron microscopy of bone marrow erythroblasts surprisingly showed most of the classical features of CDA type I. Electron microscopy may be an important tool for the diagnosis of macrocytic anemia of obscure origin, especially in young patients.

Adult↗
PubMed1991

Treatment of severe aplastic anemia with antilymphocyte globulin and androgens: a report on 33 patients.

Thirty-three patients with severe aplastic anemia were treated with antilymphocyte globulin (ALG, Mérieux) and androgens (with or without corticosteroids) between 1981 and 1989; 24 patients (72.7%) were responders after one course of ALG, eight were nonresponders, and only one patient had an early death. Eighteen of the 24 responses occurred within 2 months of ALG treatment. Of note is the good response rate we obtained for very severe aplastic anemia (four responders of five evaluable patients). With a median follow-up of 36 months (range 1-97), a survival rate of 77.6% +/- 1.2% was obtained at 30 months. No predictive factor of survival could be identified except response to treatment (p = 0.0001). The duration of the disease before treatment was inversely related to survival, although this difference did not reach statistical significance (p = 0.06). Four initial responders relapsed after 14, 24, 38, and 57 months. Three of these patients received a second course of ALG and two responded. In contrast, four of the non-responders received a second course of ALG, with only one response. Toxicity of androgens was mild. No patient developed a PNH clone or myelodysplastic syndrome. Major toxicity of corticosteroids was femoral osteonecrosis in three patients. In our experience, the combination of ALG and androgens in SAA, with or without corticosteroids, was associated with a higher response rate and better survival than in many previously published reports. This could have been due to the intensive supportive care during the initial weeks of treatment. We suggest that it may also result from the addition of androgens to ALG, although this issue may only be resolved in a randomized study.

Adolescent↗