Search PubMed⌕ Search

Biomedical subjects

D Bordessoule

Publications and source records attributed to D Bordessoule.

At least 55 records · Page 3Linked to original sources
PubMed1997

Is treatment with hydroxyurea leukemogenic in patients with essential thrombocythemia? An analysis of three new cases of leukaemic transformation and review of the literature.

From 1981 to 1995, we diagnosed, followed and treated at our institution fifty-eight cases of essential thrombocythemia (ET), using hydroxyurea (HU) as first-line therapy in these patients. Three patients who were continuously receiving HU had a leukemic transformation after a chronic phase of respectively 47, 81 and 90 months. One patient developed an acute leukemia with minimal myeloid differentiation (AML MO) and soon died of refractory disease; the second developed a refractory anemia with excess blasts in transformation (t-RAEB) and survived one year; the third patient developed a chronic myelomonocytic leukemia (CMML) and is alive at 21 months. The two former patients had complex nonrandom bone marrow karyotypic abnormalities, suggestive of therapy-related leukemia, whereas the latter one had a normal karyotype throughout the chronic and leukemic phase. These findings, together with recently published results on myeloproliferative disorders (MPD) treated with HU, suggest that this drug might be as leukemogenic as other myelosuppressive therapies in patients with ET. Longterm HU therapy should be reserved for patients in whom the treatment benefits obviously outweigh the risk of inducing leukemia.

Aged↗
PubMed1997

Cytogenetic study of 30 patients with multiple myeloma: comparison of 3 and 6 day bone marrow cultures stimulated or not with cytokines by using a miniaturized karyotypic method.

Cytogenetics in multiple myeloma (MM) cases are generally difficult to perform due to the low proliferation index of malignant plasma cells (PC) in most cases. Although IL-6 and GM-CSF stimulate the in vitro proliferation of malignant plasma cells, their usefulness for improving cytogenetic results in multiple myeloma patients remains questionable, because results which compare various culture conditions in a sufficient number of patients are not available. By using a miniaturized karyotypic method, we compared in 30 multiple myeloma patients the number and percentage of clonal abnormal mitoses obtained from 3 and 6 d bone marrow cultures performed without or with two combinations of cytokines: IL-6 + GM-CSF or IL-6 + GM-CSF + IL-2 + IL-4 + TNFalpha. The percentage of patients with an abnormal karyotype, which varied with the Durie and Salmon stage of the disease, as well as the type of numerical and structural karyotypic abnormalities that we detected, were in agreement with published results. The detection of clonal karyotypic abnormalities was better after 3d of culture without cytokine than in all other culture conditions. The higher percentage of patients at all stages of MM with an abnormal karyotype in our study (76.6%) than in previous ones (20% to 60%) is largely explained by the large number of mitoses analysed in six different culture conditions due to the use of a miniaturized karyotypic method.

Bone Marrow↗
PubMed1997

Elderly patients with aggressive non-Hodgkin's lymphoma: disease presentation, response to treatment, and survival--a Groupe d'Etude des Lymphomes de l'Adulte study on 453 patients older than 69 years.

PURPOSE: To clarify disease characteristics and optimal treatment for elderly patients with non-Hodgkin's lymphoma (NHL), we performed a randomized trial in 453 patients older than 69 years with aggressive lymphoma. PATIENTS AND METHODS: Two hundred twenty patients received cyclophosphamide 750 mg/m2, teniposide (VM-26) 75 mg/m2, and prednisone 40 mg/m2/d for 5 days (CVP) and 233 patients received CVP plus pirarubicin (THP-doxorubicin) 50 mg/m2 (CTVP), each for six courses every 3 weeks. RESULTS: The median age was 75 years. Most patients had clinically aggressive disease; 30% had one and 53% two or three adverse prognostic parameters as defined by the International Prognostic Index. More patients on the CTVP arm had an elevated lactic dehydrogenase (LDH) level, but the two groups were otherwise well balanced. CTVP treatment was more frequently associated with leukopenia, thrombocytopenia, and infectious complications. Death during chemotherapy occurred in 16% and 21% of patients on the CVP and CTVP arms, respectively (not significant). Forty percent of patients achieved a complete response (CR): 47% on CTVP and 32% on CVP (chi2 = 20.98, P = .0001). The median time to treatment failure (TTF) was 7 months for CTVP versus 5 months for CVP (log-rank test, P < .05). The median survival time was 13 months in both groups; however, the 5-year survival rate was 26% with CTVP versus 19% with CVP (chi2 = 4.68, P < .05). Lymphoma progression was the primary cause of death. CONCLUSION: Elderly patients with aggressive lymphoma have an aggressive disease with adverse prognostic parameters at the time of diagnosis. Slightly longer survival was observed for patients treated with an anthracycline-containing regimen.

Aged↗
PubMed1997

[Acquired hemophilia caused by autoantibodies against factor VIII coagulation activity. Clinical, biological study and therapeutic indications. Experience based on a study of 9 cases].

STUDY DESIGNS: To describe retrospectively the experience of the Internal Medicine and Clinical Hematology Departments of a University Hospital on adult acquired hemophilia (AH) caused by autoantibody against factor VIII coagulant (f.VIII:C) activity. Diagnosis, clinical datas, associated diseases, treatment and final outcome are described and compared to the published literature. MATERIAL AND METHODS: All cases admitted in both departments since 1989 were enrolled in the study. Clotting analyses comprised clotting times (activated partial thromboplastin time, prothrombin and thrombine times), measurements of f.VIII:C level, antifactor VIII detection and measurement by the Bethesda method assay, Search for an etiologic factor could not be standardized. All patients were followed until cure, sustained improvement, or death. RESULTS: From 1989 to 1996, AH was diagnosed in nine adult patients. Mean age was 76 +/- 24.6 years (range : 65-89) and sex ratio male to female was 2. Eight bleeding episodes occurred in seven patients, resulting consistently in severe hemorrhagic anemia and leading to hemodynamic failure in two, while two others remained asymptomatic for prolonged periods. The initial levels of f.VIII:C ranged from less than 1% to 20%, and the titers of inhibitors ranged from 0.5 to 100 Bethesda units. An underlying disease, to which the appearance of their inhibitor could be related, either concomitantly or up to 1 year later, was found in four cases including (one case each): rheumatoid arthritis, lupus erythematosus with antiphospholipid syndrome, followed by non-Hodgkin malignant lymphoma, relapsing carcinoma and, biliary tract surgery. Six acute bleeding episodes necessitated symptomatic measures, based on activated prothrombin complex concentrates in four instances, with a good response in all cases. Preparation to minor surgical operations was achieved in two asymptomatic subjects by either highly purified factor VIII concentrations infusion or intravenous 1-desamino-8-D-arginine vasopressin, with a good control of local hemostasis in each case. Three received intravenous immunoglobulins, which resulted in success in one, failure in one and, questionable response in the latter. Immunosuppression, mainly with corticosteroids, cyclophosphamid, or both, was given to seven, resulting in disappearance of inhibitor in five (delay to cure ranged from 2 weeks to 10 months), improvement in one, and failure in one (in this latter case, cure was eventually achieved with the anti-Hodgkin disease MOPP chemotherapy). After a 27-month mean follow-up, six patients experienced a sustained complete response and one a sustained partial response to immuno-suppression, two untreated patients remained asymptomatic, two died later from malignancy (carcinoma and myelodysplastic syndrome). CONCLUSION: AH usually presents as a severe or even a life-threatening disease, necessitating prompt and thorough symptomatic measures directed at the cessation of bleedings and prevention of their relapse. In our experience, no death was attributable to AH or its treatment. Immunosuppression is useful in selected cases, but must be carefully discussed, since it can be highly toxic, especially in the elderly. Given the possibility of a delayed onset of some etiologic factors, a prolonged surveillance of each case of idiopathic AH is mandatory.

Aged↗
PubMed1996

Link between peripheral neuropathy and monoclonal dysglobulinemia: a study of 66 cases.

The association of peripheral neuropathy (PN) and monoclonal dysglobulinemia has often been reported, although a direct link between the two is not readily established. Linkage is generally based on consideration of the clinical, electrophysiological and immunological findings along with details of the course. We report here a study of 66 of our own cases which benefitted from immunological and immunopathological analyses of serum. In 62 of these cases, histological and immunopathological examinations of nerve biopsy specimens were realized. Such a discussion about a link between the dysglobulinemia and the peripheral neuropathy is of clinical interest as it provides information for decisions about the continuation of potentially neurotoxic chemotherapy. In this prospective study conducted on a case by case basis, the origin of the neuropathy, whether due to the chemotherapy, the dysimmune process, the presence of abnormal immunoglobulins in the nerve, amyloid deposits, infiltration of nerve parenchyme by abnormal cells, or a combination of one or more of these mechanisms, could be determined in most cases. We divided our population of 66 patients into 4 etiological groups: group 1: direct link (56.1%), group 2: indirect link (12.7%), group 3: no link (10.6%), group 4: doubtful link (21.2%). In group 1 we found a statistically significant association between the peripheral neuropathy and an IgM kappa MGUS.

Humans↗
PubMed1996

Deletion of chromosome 20q associated with hypereosinophilic syndrome. A report of two cases.

Deletion of the long arm of chromosome 20--del(20q)--is commonly associated with myeloid malignancies, in particular with myeloproliferative disorders (MPD), myelodysplastic syndrome (MDS), and acute myelogenous leukemia (AML). Its association with the hypereosinophilic syndrome (HES) had never been reported. In the present study we describe two patients with long-standing hypereosinophilia and features of atypical MPD or MDS carrying a del(20q) as a constant and isolated chromosomal abnormality. One patient, with an aggressive clinical course, died within 2 years, despite several lines of treatment. The other patient had a more indolent course consistent with that of an atypical MDS with eosinophilia.

Aged↗
PubMed1996

Effect of granulocyte colony-stimulating factor administration in elderly patients with aggressive non-Hodgkin's lymphoma treated with a pirarubicin-combination chemotherapy regimen. Groupe d'Etudes des Lymphomes de l'Adulte.

PURPOSE: Results of a multidrug chemotherapy regimen consisting of cyclophosphamide, pirarubicin, teniposide, and prednisolone (CTVP) plus subcutaneous granulocyte colony-stimulating factor (G-CSF) in elderly patients with aggressive non-Hodgkin's lymphoma (NHL) are reported. PATIENTS AND METHODS: Between January and December 1992, 46 previously untreated patients older than 69 years with intermediate- and high-grade NHL received cyclophosphamide 750 mg/m2, teniposide 75 mg/m2, pirarubicin 50 mg/m2 day 1, and prednisolone 40 mg/m2 days 1 to 3. G-CSF, 5 micrograms/kg/day, was administered from day 4 up to day 14 or when the absolute neutrophil count reached 5 x 10(9)/l. Six cycles were scheduled every 3 weeks. RESULTS: Grade 3 or grade 4 neutropenia complicated 22% and 26% of chemotherapy cycles, respectively. Fever or/and clinical infection were observed in 4% and 14% of cycles. One toxic death related to a septic shock occurred. Eight cycles (4%) were delayed with a median duration of 7 days. Administered median dose intensity was 93.5%. Objective response rate was 74% and 46% of the patients achieved a complete response. The 2-year overall survival and event-free survival rates were 47% and 28%. CONCLUSION: In comparison with a previous group of patients treated with CTVP, G-CSF allows delivery of chemotherapy with a reduced neutropenia-induced morbidity in an outpatient setting in elderly patients with aggressive NHL without modifying response rate or survival.

Aged↗
PubMed1996

Phase II trial of fludarabine monophosphate as first-line treatment in patients with advanced follicular lymphoma: a multicenter study by the Groupe d'Etude des Lymphomes de l'Adulte.

PURPOSE: Fludarabine monophosphate (FAMP) is a major drug in the treatment of chronic lymphocytic leukemia and showed efficacy in selected groups of patients with low-grade lymphomas, most of them pretreated. The aim of this trial was to assess the efficacy and the toxicity of FAMP in untreated patients with follicular lymphoma. PATIENTS AND METHODS: Fifty-four untreated patients with advanced follicular lymphoma were treated with intravenous (i.v.) fludarabine at a dose of 25 mg/m2/d during 5 days every 4 weeks, to a maximum of nine cycles. RESULTS: The toxicity of the drug was mild, mainly granulocytic. Granulocytopenia > or = 3 (World Health Organization [WHO]) was observed during 48 of 328 cycles (14.6%) and in 22 of 53 (41%) patients assessable for toxicity. Fludarabine had to be stopped prematurely because of toxicity in nine patients: marrow toxicity in five, peripheral neuropathy in two, and interstitial pneumonitis and hepatitis in one patient each. Among 49 patients assessable for response, the overall response rate was 65% and the complete response (CR) rate 37%. The median progression-free survival interval for all patients was 13.6 months. CONCLUSION: These results confirm that fludarabine is active when used as first-line treatment in patients with follicular lymphoma and has a low toxicity rate. It may be used as single treatment in elderly patients. Associations of fludarabine with other drugs active against follicular lymphoma need to be determined.

Adult↗
PubMed1996

[Treatment of accidental extravasation of antitumor agents with dimethylsulfoxide and alpha-tocopherol].

INTRODUCTION: The aim of this study was to test topical applications of dimethylsulfoxide and alpha-tocopherol for the prevention of ulcerations after antimitotic extravasation. METHODS: An open prospective study was conducted in 10 patients in 4 different chemotherapy wards who had experienced infusion accidents leading to phlebitis (4 cases) or cellulitis (8 cases) including 2 at implant sites. Topical application of the dimethylsulfoxide alpha-tocopherol combination was initiated within the first hours and continued for 3 to 15 days. One patient was given dimethylsulfoxide alone. RESULTS: Necrosis was never observed. The implant sites were preserved and remained functional. CONCLUSION: The absence of secondary ulcerations and the preservation of the implant sites are clear advantages of this topical combination which should be used as first line treatment. Favorable results have been reported in the literature while other techniques used depend on the antimitotic agent and give variable results.

Administration, Topical↗
PubMed1995

A controlled study of recombinant human granulocyte colony-stimulating factor in elderly patients after treatment for acute myelogenous leukemia. AML Cooperative Study Group.

BACKGROUND: Intensive chemotherapy for acute myelogenous leukemia (AML) continues to yield low rates of complete remission and survival among patients over the age of 65 years. Infection-related mortality is particularly high among these patients during the period of neutropenia that follows chemotherapy. We determined the effect of lenograstim (glycosylated recombinant human granulocyte colony-stimulating factor) on mortality at eight weeks (the main end point) and the rate of complete remission among patients with AML who were 65 years old or older. METHODS: After induction chemotherapy with daunorubicin (45 mg per square meter of body-surface area per day for 4 days) and cytarabine arabinoside (200 mg per square meter per day for 7 days), 173 patients with newly diagnosed AML were randomly assigned on day 8 to receive either lenograstim (5 micrograms per kilogram of body weight per day) or placebo, starting on day 9, until there was neutrophil recovery or a treatment failure, or for a maximum of 28 days. Salvage chemotherapy was also followed by lenograstim or placebo. Patients with a complete remission received two consolidation courses of chemotherapy without lenograstim or placebo. RESULTS: The mortality rate at eight weeks was similar in the lenograstim and placebo groups (23 and 27 percent, respectively; P = 0.60), as was the incidence of severe infections. The median duration of neutropenia (absolute neutrophil count < or = 1000 per cubic millimeter) was shorter in the lenograstim group (21 days, as compared with 27 days in the placebo group; P < 0.001). Eight percent of the patients in both groups had regrowth of AML cells. The rate of complete remission was significantly higher in the lenograstim group (70 percent, as compared with 47 percent in the placebo group; P = 0.002). Overall survival, however, was similar in the two groups (P = 0.76). CONCLUSIONS: The administration of lenograstim after chemotherapy for AML did not decrease the mortality rate at eight weeks among patients over the age of 65 years. The patients who received lenograstim had a significantly higher rate of complete remission than those who received placebo. Nevertheless, the overall survival in the two groups did not differ significantly.

Adjuvants, Immunologic↗
PubMed1995

Non-Hodgkin malignant lymphomas and peripheral neuropathies--13 cases.

Non-Hodgkin's malignant lymphomas (NHML) are malignant lymphoid proliferations which may be of B or T cell type. Thirteen observations of an association between peripheral neuropathy and B type NHML are reported. None of the cases had evidence of meningeal propagation or neurotoxicity from chemotherapy. The NHML were classified according to the Working Formulation and Kiel classifications. The various mechanisms of peripheral neuropathy in these cases were split into four broad groups. Group I consisted of four cases in which the peripheral nerve lesions were directly linked to a propagation of malignant cells into the peripheral nervous system; this was revealed by autopsy and/or nerve biopsy. Malignant B cell proliferation was demonstrated in three out of four of these cases by immunolabelling of the infiltrates. Group II included three patients whose serum contained a monoclonal immunoglobulin (IgM) with antimyelin activity, and two who had pathological IgM deposits in endoneurial connective tissue. Group III comprised two cases. The immune dysfunction of the NHML was responsible for a Guillain-Barré syndrome in one, and for a chronic inflammatory demyelinating polyneuropathy in the other. Group IV included two patients in whom the mechanism of the peripheral neuropathy, although almost certainly directly related to the NHML, could not be determined beyond doubt. The peripheral neuropathy might have been a result of a paraneoplasic process or, possibly, an undetected lymphomatous invasion of nervous tissue. All these cases of clinically diverse peripheral neuropathy, which either occurred before the discovery of the haemopathy or arose as complications of it, are discussed along with similar observations reported in the literature. Immunolabelling of lymphomatous proliferations and nerves is now of considerable value for classifying and indicating the exact aetiology of the peripheral neuropathy. It can also detect pathogenic consequences of any associated monoclonal dysglobulinemia. In any event, a direct link between the peripheral neuropathy and NHML represents an indication for intensification of specific chemotherapy, which in some of our patients led to significant regression of the peripheral neuropathy. Nonetheless, in some cases, the link between peripheral neuropathy and NHML could not be established with certainty. Long-term follow-up is essential in such cases. The present results show the importance of a case by case study of patients with NHML and peripheral neuropathy.

Aged↗
PubMed1995

AcSDKP serum concentrations vary during chemotherapy in patients with acute myeloid leukaemia.

AcSDKP is a physiological negative regulator of cell proliferation in mammals. In Ara-C-treated mice its plasmatic concentrations decrease while the CFU-S start cycling. Infusion of AcSDKP protects these animals from death by blocking the proliferation of primitive haemopoietic cells. We measured AcSDKP serum concentrations in 20 AML patients during the course of high-dose cytoreductive treatment. We observed an early and sharp increase of AcSDKP during the induction treatment in 12 patients, reaching a peak during the initial 3 d of treatment in nine of them. These results are contrary to those observed in mice treated with high doses of Ara-C. They encourage further clinical investigation, and suggest that treatments with synthetic AcSDKP (Seraspenide) will perhaps have to be adjusted to the type of disease and the schedule of chemotherapy in order to optimize its myeloprotective effect.

Acute Disease↗
PubMed1993

[Peripheral neuropathies and hemopathies].

In our experience, the incidence of an association between peripheral neuropathy and hemopathy is around 7%. The corresponding nerve involvement may reveal or complicate a known hemopathy. The exact cause-effect relationship is not always easy to identify. We discuss here the peripheral nerve complications of acute leukemia, myeloproliferative disorders, monoclonal dysglobulinemia, non-Hodgkin's malignant lymphoma and Hodgkin's disease. The peripheral neuropathy arising in cases of monoclonal dysglobulinemia, non-Hodgkin's malignant lymphoma have most benefited from ultrastructural examination and advances in immunological and immunocytochemical techniques. Accurate determination of the lesional mechanism should help devise appropriate therapeutic strategies.

Dysgammaglobulinemia↗
PubMed1993

Immunohistological patterns of myeloid antigens: tissue distribution of CD13, CD14, CD16, CD31, CD36, CD65, CD66 and CD67.

A number of differentiation antigens on myeloid cells have been defined on the CD classification system by the four International Workshops on Human Leucocyte Differentiation Antigens. The distribution of eight of these antigens (CD13, CD14, CD16, CD31, CD36, CD65, CD66, CD67) have been studied in human tissues, with the aim of documenting their immunohistological patterns and their degree of myeloid restriction. CD13, the most widely distributed antigen, was found in skin, bile canaliculi, kidney and pancreas. CD14 was not restricted to monocytes and tissue macrophages, being also strongly expressed on dendritic reticulum cells. CD16 was expressed on granulocytes and tissue macrophages (alveolar and Kupffer cells) and in the red pulp of the spleen. CD31 and CD36 gave a characteristic staining of vascular endothelium, corresponding to their identification as the platelet glycoproteins gp IIa and gp IV. Antibodies against the most recently defined myeloid antigens (CD65, CD66 and CD67) appeared to be more specific for myeloid differentiation than previously described 'myeloid antigens'.

Antibodies, Monoclonal↗