Search PubMed⌕ Search

Biomedical subjects

M C Pike

Publications and source records attributed to M C Pike.

At least 325 records · Page 18Linked to original sources
PubMed1973

Immunosuppressive consequences of radiotherapy and chemotherapy in patients with acute lymphoblastic leukaemia.

Assays of lymphocyte subpopulations and function have been performed on patients with acute lymphoblastic leukaemia still in remission after 18 months' treatment. The patients were subjects of a trial of the value of craniospinal irradiation in the third month of treatment in preventing central nervous system relapse. Effects of both irradiation and chemotherapy were observed. Lymphopenia was much more marked in those patients who had received irradiation over a year previously. Assays of response to phytohaemagglutinin (P.H.A.) and staining for surface immunoglobulin indicated that this difference was due to a deficiency in thymus-dependent lymphocytes in the irradiated children. Chemotherapy had a particularly marked depressant effect on lymphocytes with antibody-dependent cytotoxic activity and a proportion of PHA-responsive cells were also depressed. It may be relevant that four of the patients depleted of thymus-dependent lymphocytes by radiation died of infection during remission, while none of those treated with chemotherapy alone died in remission.

Child↗
PubMed1972

Factors in pathogenesis of central-nervous-system leukaemia.

Eighty-three (50%) of 165 children with acute lymphoblastic or acute stem-cell leukaemia presenting during 1958-70 developed leukaemia of the central nervous system (C.N.S.). The rate of incidence of this complication is fairly constant throughout the first two-and-a-half years of the disease, but falls thereafter. The incidence of C.N.S. leukaemia is inversely correlated with the platelet count at the time of initial diagnosis of leukaemia, and directly correlated with the total leucocyte count and the presence of lymph-node enlargement. The major effect of initial leucocyte count is on the time of onset of clinical symptoms. It is suggested that leukaemic cells usually enter the C.N.S. from the blood as a result of intracranial petechial haemorrhage occurring around the time of initial diagnosis of leukaemia, and that the time for subsequent development of symptoms of C.N.S. disease is largely determined by the number and replication rate of leukaemic cells which gain access to the C.N.S. at that time. The increasing frequency of diagnosis of C.N.S. leukaemia in recent years is not wholly explained by increasing survival, and may in part be related to changes in the pattern of antileukaemic therapy.Prophylaxis for C.N.S. leukaemia should be instituted as early as practicable after diagnosis; the identification of a high-risk group may permit this to be done selectively.

Blood Cell Count↗