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Biomedical subjects

M Hayat

Publications and source records attributed to M Hayat.

At least 73 records · Page 4Linked to original sources
PubMed1991

Pericarditis and myocardial infarctions after Hodgkin's disease therapy.

From 1971 to 1984, 499 patients with all stages of Hodgkin's disease received mediastinal irradiation at the Institut Gustave-Roussy by 25 MV photons from a linear accelerator. Thirty-five pericarditis (10-year cumulative incidence rate of 9.5%) and 13 myocardial infarctions (MI) (10-year cumulative incidence rate of 3.9%) were observed. In contrast, no cases were diagnosed in a parallel series of 138 Hodgkin's disease patients treated without mediastinal irradiation during the same period of time (p less than 0.005 for pericarditis, p less than 0.05 for MI). By multivariate analysis, the role of total radiation dose given to the mediastinum and that of fraction size were evaluated, adjusting for age, sex, mediastinal involvement, and type of chemotherapy. The pericarditis risk was significantly increased with total dose greater than or equal to 41 Gy (relative risk (RR) = 3.25, p = 0.006) and with dose per fraction greater than or equal to 3.0 Gy (RR = 2.0, p = 0.06). The myocardial infarction risk was not found to be related to total dose nor to fraction size in this series, possibly because of the small number of events.

France↗
PubMed1991

[Prolymphocytic leukemia].

Prolymphocytic leukemia is an entity characterized by morphologic, immunologic, clinical and behavioral features which allows its keeping apart from chronic lymphoid leukemia. Careful analysis of blood smear is the main step for its diagnosis. Our purpose is to remind this particular chronic lymphoproliferative syndrome which requires energetic initial treatment. Prolymphocytic leukemia de novo as well as a possible transformation of chronic lymphoid leukemia to prolymphocytic leukemia are discussed.

Adult↗
PubMed1991

[Immediate hematologic tolerance of extended irradiations after chemotherapy. Apropos of 78 cases of Hodgkin's disease stage III and IV without marrow involvement treated at the Gustave-Roussy Institute].

Early hematotoxicity following 4 to 8 courses of polychemotherapy has been analysed in 78 patients (mean age 32.5 years) treated for advanced stage Hodgkin's disease (53 stages III, 25 stages IV). Toxicity occurred in a third of the patients, and led to interrupt the treatment in one case out of 7, definitively in half of them. The thrombocyte lineage appeared the most sensitive to irradiation. Toxicity was proportional to the target volume (42% of upper and infra-diaphragmatic field versus 11.5% of one sided irradiation, P = 0.01). Toxicity was more frequent after infra-diaphragmatic irradiation (32% of para-aortic field, 43.75% of inversed Y field) than after mantle field (12.3%, P = 0.01). Tolerance to extended field irradiations seemed better in young patients. Sex, stage, type of chemotherapy did not influence toxicity in our series. Abnormalities of the blood count before irradiation was predictive of toxicity. While expecting development of megakaryocytic growth factors of autologous bone marrow transplantation, we suggest: 1) to achieve total lymphoïd irradiation in three periods (mantle field then lombo-aortic field-/+ spleen, then iliac and inguinal fields); 2) to wait, if possible, until normalization of the hemogram before starting the irradiation.

Adolescent↗
PubMed1990

Gene transfer, expression and inheritance of pRSV-rainbow trout-GH cDNA in the common carp, Cyprinus carpio (Linnaeus).

A recombinant plasmid containing the Rous sarcoma virus-long terminal repeat (RSV-LTR) promoter linked to rainbow trout (Salmo gairdneri) growth hormone (GH) cDNA was microinjected into fertilized carp eggs. Genomic DNA extracted from pectoral fin of individual presumptive transgenic fish was analyzed by dot blot and Southern blot hybridization, using the RSV-LTR and/or the GH cDNA sequences as probes. Out of 365 presumptive transgenic fish analyzed, 20 individuals were found to contain pRSV-rtGH-cDNA sequence in the genomic DNA. Expression of the trout GH polypeptide was detected by immunobinding assay in the red blood cells of nine transgenic fish tested. The level of expression, however, varied among the transgenics and could not be correlated with exogenous DNA copy number. Although there was considerable variation in the sizes of the transgenic fish, those microinjected during the one-cell stage were (P less than 0.05) 22% larger, on the average, than their sibling controls. A randomly selected fraction of the progeny derived from crosses between transgenic males and non-transgenic females inherited the foreign DNA. These transgenic progeny grew faster (P less than 0.05) than their non-transgenic siblings.

Animals↗
PubMed1990

Immunoscintigraphy of Hodgkin's disease: in vivo use of radiolabelled monoclonal antibodies derived from Hodgkin cell lines.

The Hodgkin associated monoclonal antibody (Mab) HRS-1 reacts with Hodgkin and Reed-Sternberg cells (HR-S) in all HD subtypes. HRS-1 Mab was labelled with radioiodine and injected into 10 patients for immunoscintigraphy (IS). Seven patients were injected with HRS-1 Mab radiolabelled with 131I and three patients were injected with HRS-1 Mab labelled with 123I. A control anti-alpha-fetoprotein (anti-AFP) Mab was radiolabelled with another iodine isotope and was injected simultaneously in five cases. Six out of eight patients with proven HD had a true positive scan (nodal, splenic and bony involvement). Imaging was equivocal or failed in the two other patients. In the last two patients IS imaging was truly negative due to the absence of residual HD in one patient and to an erroneous histological diagnosis of HD in another patient. These results, although preliminary, demonstrate that IS with radioiodine-labelled HRS-1 Mab is feasible and may prove to be informative in the staging of HD.

Animals↗
PubMed1990

Causes of death after therapy for early stage Hodgkin's disease entered on EORTC protocols. EORTC Lymphoma Cooperative Group.

The risk of dying from different causes after Hodgkin's disease (HD) therapy has been quantified from a series of 1,449 patients with early stages included in four successive clinical trials conducted by the European Organization for Research and Treatment of Cancer (EORTC) Lymphoma Cooperative Group since 1963. Overall, 240 patients died and the 15-year survival rate was 69% whereas the expected rate was 95%. The standardized mortality ratio (SMR) technique was used to quantify excess deaths as a function of time since first therapy. At each interval, SMR was significantly increased, giving: 0-3 year, 8.86 (p less than 0.001); 4-6 year, 9.25 (p less than 0.001); 7-9 year, 7.08 (p less than 0.001); 10-12 year, 9.53 (p less than 0.001); 13-15 year, 4.37 (p less than 0.01); and 16+ years, 3.80 (p less than 0.05). While the proportion of deaths as a consequence of HD progression, treatment side-effect, and intercurrent disease decreased with time, that of second cancer and cardiac failure peaked during the 10-12 year post-treatment interval. After 15 years of follow-up, the risk of dying from causes other than HD continued to increase. These findings indicate that although probably cured from HD, patients are at higher risk for death than expected, a risk that might be a consequence of therapy.

Adult↗
PubMed1990

Salvage therapy with methyl-gag, high-dose Ara-C, M-Amsa, and ifosfamide (MAMI) for recurrent or refractory lymphoma.

Thirty adult patients with relapsed or refractory malignant lymphoma underwent a Phase I-II trial of salvage chemotherapy combining methyl-gag, high-dose Ara-C, M-Amsa, and ifosfamide (MAMI protocol). All patients had been extensively pretreated. At the time of salvage therapy, 21 patients had visceral involvement and 23 patients were refractory. The overall response rate was 50% (11 patients in complete remission and 3 patients in partial remission). The main toxicity was myelosuppression; 4 treatment-related deaths occurred and 17 patients died of tumor progression with a median of 5 months. The MAMI protocol showed similar antitumoral efficacy to that of other salvage chemotherapy regimens used for poor prognosis malignant lymphoma but was more toxic. However, a response rate of 45% in refractory patients should be taken into account and this drug association deserves further investigation with regard to the selection of patients for bone marrow transplants.

Adolescent↗
PubMed1990

[Cancer of the bladder after treatment with cyclophosphamide. Apropos of a case and a review of the literature].

A case of cancer of the bladder is reported in a patient treated 5 years previously with cyclophosphamide for membranoproliferative glomerulonephritis. The responsibility of cyclophosphamide for this type of tumour is well documented in the literature and should lead to a limitation of its use in disease with a favourable prognosis and to close surveillance via regular cystoscopy and blind biopsy in patients who receive more than 50 g of the drug.

Adult↗
PubMed1990

[Chemotherapeutic intensification in germ cell tumors].

Chemotherapy has dramatically improved the prognosis of non-seminomatous germ cell tumors (NSGCT). However, some patients relapse and others are refractory to first line chemotherapy. We studied a salvage chemotherapeutic regimen with etoposide 75 gm/m2/day, and cisplatin 40 mg/m2/day, days 1-5 and Ifosfamide 3 g/m2/day, days 1 and 2 (VIhP regimen) in 32 patients. We observed 8 complete remissions with 4 long-term NED patients. Hematological, neurological and renal complications were frequent. In 16 other cases, a protocol using high dose chemotherapy, followed by autologous bone marrow rescue was studied. We observed 8 complete remissions with 4 long-term NED patients. These observations support a dose/effect relationship. A French randomized trial testing high dose chemotherapy, followed in some cases by an autologous marrow graft in poor risk advanced NSGCT, has recently been activated.

Adolescent↗
PubMed1989

[Intensive induction and early consolidation of acute lymphoid leukemia in the adult. A pilot study of feasibility and long-term development].

Between April and December, 1982, a multicentre pilot study was conducted in 45 patients aged from 16 to 73 years suffering from acute lymphoblastic leukaemia to test the feasibility of an intensive and short induction phase followed by an early consolidation phase. All patients received a 5-day course of induction chemotherapy with prednisone, vincristine, AraC and rubidazone, then a "triple A regimen" for consolidation, consisting of adriamycin, AraC and asparaginase. The complete remission rate was 73 per cent. Toxicity during induction was characterized by frequent infections, but the consolidation treatment was well tolerated. Thus, the sequence intensive induction-early consolidation proved feasible and acceptable. In terms of survival, 8 out of the 33 patients in remission are still alive and well after more than 4 1/2 years.

Adolescent↗
PubMed1989

Very late recurrence of childhood acute lymphoblastic leukemia treated with chemoimmunotherapy: a report of three cases occurring 19, 11, and 9 years after discontinuation of chemotherapy.

Current therapeutic modalities for childhood acute lymphoblastic leukemia (ALL) are associated with a high cure rate, and recurrences more than 4 years after therapy cessation are very unusual. We report three cases of exceptionally late recurrences of childhood ALL after cessation of chemotherapy (CT) given for respective periods of 8, 7, and 24 months. CT was followed by maintenance immunotherapy (IMT) with Bacillus Calmette-Guérin (BCG) and allogeneic leukemic lymphoblasts pretreated with formaldehyde or irradiated in vitro. Leukemic recurrences were observed 19, 11, and 9 years after cessation of CT and appeared morphologically similar to the original blasts. A second complete remission was easily achieved in all three patients, but two went on to repeated relapse (one has died following the fourth recurrence). We speculate that some residual leukemic cells, remaining after the inadequate, short-term CT, were responsible for these unusual evolutions, and we question a possible delaying role of IMT in prolonging remission. Other possible etiologies are discussed.

Antineoplastic Combined Chemotherapy Protocols↗