Clinical & Laboratory HaematologyVolume 1, Issue 2 p. 87-94 Free Access Acute lymphoblastic leukaemia of B cell origin S. ROATH MD, FInst Biol, FRCPath, S. ROATH MD, FInst Biol, FRCPath Faculty of Medicine, University of SouthamptonSearch for more papers by this author S. ROATH MD, FInst Biol, FRCPath, S. ROATH MD, FInst Biol, FRCPath Faculty of Medicine, University of SouthamptonSearch for more papers by this author First published: June 1979 https://doi.org/10.1111/j.1365-2257.1979.tb00456.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References ACAR S., TEKINALP G., IZSOYLU S., CEVIK N. & YASAR H. (1977) Burkitt's lymphoma cell leukemia. Acta Haemat. 57, 188. BARRETT S. G., SCHWADE J. G., RANKEN R. & KADIN M. E. (1977) Lymphoblasts with both T and B markers in chilhood leukemia and lymphoma. Blood 50, 71. BENNETT J. M., CATOVSKY D., DANIEL M. T., FLANDRIN G., GALTON D. A. G., GRALNICK H. R. & SULTAN C. (1976) Proposals for the classification of the acute leukaemias. French-American-British (FAB) co-operative group. Brit. J. Haemat. 33, 451. BELPOMME D., MATHE G. & DAVIES A. J. S. (1977) Clinical significance and prognostic value of the T and B immunological classification of human primary acute lymphoid leukaemia. Lancet I, 555. BROUET, J. C., VALENSI, F., DANIEL, M. T., FLANDRIN, G., PREUD'HOMME, J. L. & SELIGMAN, M. (1976) Immunological classification of acute lymphoblastic leukaemias. Evaluation of its clinical significance in 100 patients. Brit. J. Haemat. 33, 319. BROUET J. C., PREUD'HOMME J. L., SELIGMAN M. & BERNARD J. (1973) Blast cells with monoclonal surface immunoglobulins in 2 cases of acute blast crisis supervening on chronic lymphocytic leukaemia. Brit. med. J. iv, 23. BROWN G., HOGG N. & GREAVES M. (1975) Candidate leukaemia-specific antigen in man. Nature 258, 454. CATOVSKY D., CALETTO J., OKOS A., MILIANI E. & GALTON D. A. G. (1974) Cytochemical profile of B and T leukaemic lymphocytes with special reference to acute lymphoblastic leukaemia. J. din. Path. 27, 767. CATOVSKY D., GALETTO J., OKOS A., WILTSHIRE E., GALTON D. G. & STATHOPOULOS G. (1973) Prolymphocytic leukaemia of B and T cell type. Lancet ii, 232. CHESSELS J. M., HARDISTY R. M., RAPSON N. T. & GREAVES M. F. (1977) Acute lymphoblastic leukaemia in children. Classification and prognosis. Lancet ii, 1307. CIMINO M. C., ROTH D. G., GOLOMB H. M. & ROWLEY J. D. (1978) A chromosome marker for B-cell cancer. N. Engl. J. Med. 298, 1422. DAVEY, F. R. & GOTTLIEB, A. J. (1974) Lymphocytic surface markers in A. L. L. Am. J. din. Path. 62, 818. DAVIS S. (1976) The variable pattern of circulating lymphocyte subpopulations in chronic lymphocytic leukemia. N. Eng. J. Med. 294, 1150. DOW L. W., BORELLA L., SEN L., GEORGE S. L., MAUER A. M. & SIMONE J. V. (1977) Initial prognostic factors and lymphoblast-erythrocyte rosette formation in 109 children with A. L. L. Blood 50, 671. EDEN O. B. & INNES E. M. (1978) Cell surface markers in lymphoblastic leukaemia Lancet ii 378. FERRARINI M., TONDA G. P., RISSO A. & VIALE G. (1975) Lymphocyte membrane receptors in human lymphoid leukaemias. Em. J. Immunol. 5, 89. FLANDRIN G., BROUET J. C., DANIEL M. T. & PREUD'HOMME J. L. (1975) Acute leukemia with Burkitt's tumour cells: A study of 6 cases with special reference to lymphocyte surface markers. Blood 45, 183. FU S. M., WINCHESTER R. S. & KUNKEL H. G. (1976) The occurrence of the HL-B alloantigens on the cells of unclassified acute lymphoblastic leukaemias. J. exp. Med. 142, 1334. GAJL-PECZALSKA, K. J., BLOOMFIELD, C. D., NESBIT, M. E. & KENSEY, J. M. (1974) B-cell markers on lymphoblasts in acute lymphoblastic leukaemia. Clin. exp. Immunol. 17, 561. GARCIA J. C., YI-HSIANG C. & HSU C. C. S. (1977) Lymphocyte surface markers in acute lymphoblastic leukemia of adults. Am. J. din. Path. 68, 543. HAEGERT D., CAWLEY J. C., KARPAS K. & GOLDSTONE A. M. (1974) Combined T and B cell acute lymphoblastic leukaemia. Brit. med. J. 4, 79. HEIDEMAN R. L., FALETTA J. M., MUKHOPADHYAY M. S. & FERNBACH D. J. (1978) Lymphocytic leukemia in children. Prognostic significance of clinical and laboratory findings at time of diagnosis. J. Pediat. 92, 540. HUTTON J. J., COLEMAN M. S., GREENWOOD M. F., HOLLAND P., LAMPKIN B. & KOILL C. (1979) Adenogene deaminase, terminal transferase and cell markers in acute lymphoblastic leukaemia. Blood 50, (Suppl.) 193 (abst.). HSU C. C. S. & MORGAN E. R. (1978) Detection of B lymphocyte (B cell) associated antigens on human leukaemic lymphocytes. Am. J. Path. 70, 741. JANOSSY G., GOLDSTONE H., CAPARELLO D., GREAVES M. F., KULENKAMPFF J., PIPPARD M. & WELSH K. (1977) Differentiation linked expression of p28, 33 (la-like) structures on human leukaemic cells. Brit. J. Haemat 37, 391. JAYASWAL U., ROATH S., HYDE R. D., CHISHOLM D. M. & SMITH J. L. (1977) Blood lymphocyte surface markers and clinical findings in chronic lymphoproliferative disorders. Brit. J. Haemat. 37, 207. KADIN M. E. & BILLING R. J. (1977) Immunofluorescent method for positive identification of null-cell type acute leukemias.; Use of the heterologous antiserum. Blood 50, 771. KAPLAN J., RAVINDRANATH Y. & PETERSON W. D. JR (1977) T and B lymphocyte antigen-positive null cell leukemias. Blood 49, 371. KISLIAK N. S., IZOTOVA T. A., SOKOLOV P. P., LENDKAIA R. V. & BASISTOVA A. A. (1977) A case of acute lymphoid leukaemia with proliferation of cells possessing the properties of B-lymphocytes. Probl. Cemetol. Pereliv. Krovi. 22, 50. KUMAR S., CARR T. F., EVANS D. I. K., MORRIS-JONES P. & HANN I. M. (1979) Prognostic significance of cell surface markers in childhood acute lymphoblastic leukaemia. Clin. lab. Haemat. I, 121. MOHANSKUMAR T. & RANEY R. B. (1978) Leukaemia associated antigens in man. In Clinics in Haematotogy, Vol. 7, no. 2, Acute Leukaemia, ed. J. V. Simone, p. 363. W. B. Saunders, Eastbourne . NAKAZAWA S., MINOWADER J. & SINKS L. F. (1976) Receptors for sheep erythrocytes (E) and erythrocyte-antibody-complement complexes (EAC) on the lymphoblasts of childhood acute lymphoblastic leukemia. Med. pediatr. Oncol. 2, 147. OSHIMURA M., FREEMAN A. I. & SANDBERG A. A. (1977) Chromosomes and causation of human cancer of leukemia XXVI binding studies in A. L. L. Cancer 40, 1161. ROATH S. (1964) The acute leukaemias: A study of 580 cases. Q. J. Med. 33, 257. ROATH S., NEWELL D. G., POLLIACK A., ALEXANDER E. & LIN P. (1978) Scanning electron microscopy and the surface morphology of human lymphocytes. Nature 273, (5657) 15. SAMOI LOVA R. S., BULICHEVA T. I. & SKURKOVICH S. V. (1975) Immunoglobulins on the surface of blast cells in human leukemias. Blood 46, 443. SHAW M. T., PALMER C. & YUHARS J. M. (1977) Characteristics of a Burkitt-like leukaemia in a 71 year old woman. Blood 50, (Suppl.) 209 (abst). SMITH J. L., NEWELL D. G., GORDON J., ANSON A. & ROATH S. (1979) B cell acute lymphatic leuk aemia. Immunoglobulin synthesis, morphology and clinical features. Scand. J. Haemat. 22, 246. TSUKIMOTO I., WONG K. Y. & LAMPKIN B. S. (1976) Surface markers and prognostic factors in A. L. L. N. Engl. J. Med. 294, 245. VOGLER L. B., CRIST W. M., BOCKMAN D. E., PEARL E. R., LAWTON A. R. & COOPER M. D. (1978) Pre-B-cell leukaemia. A new phenotype of childhood lymphobastic leukemia. N. Engl. J. Med. 298, 872. WOLFF L. J., RICHARDSON S. T., NEIBERGER J. B., NEIBERGER R. G., IRWIN D. S. & BACHEUR R. L. (1976) Poor prognosis of children with A. L. L. and increased B cell markers. J. Pediat. 89, 956. ZECH L., HAGLUND U. & NILSSON K. (1976) Characteristic chromosomal abnormalities in biopsies and lymphoid-cell lines from patients with Burkitt and non-Burkitt lymphomas. Int. J. Cancer 17, 47. Volume1, Issue2June 1979Pages 87-94 ReferencesRelatedInformation

Viability studies on lymphocytes labelled with indium In111 using oxine as a ligand showed impairment as measured by trypan-blue assessment and rosetting ability. In addition, lymphocyte response to phytohaemagglutinin stimulation as measured by tritiated-thymidine uptake was also impaired at levels where adequate cell labelling had taken place. Cadmium toxicity was not noticed, and the use of tropolone as a ligand offered possibilities of reduced cellular toxicity. Such cytotoxicity may not have been important in earlier reported studies on granulocytes where the large numbers available for in vivo work and the short periods of study still allowed useful conclusions to be drawn. However, because of the prolonged lifespan of the human lymphocyte, the cytotoxic effects of the processing might well make the long-term studies which would be of interest much less reliable for clinical assessment.

Lymphadenopathy is an uncommon finding in hairy cell leukaemia (HCL). We report 12 HCL patients in whom relapse was associated with massive abdominal lymphadenopathy. All but one had long-standing HCL (range 3-25 years; median 10 years); in one it was discovered at presentation. Nine patients had been splenectomized and seven had previously been treated with 2'deoxycoformycin (DCF) and/or alpha-interferon (alpha IFN): three had achieved complete remission and four a partial response. The computerized tomography (CT) scan appearances were similar in all cases with a primary lymph node mass centred around the coeliac axis and involving upper para-aortic and retropancreatic regions. Histology and/or cytology confirmed nodal involvement by HCL in six patients. Large immature hairy cells were seen in both lymph nodes and bone marrow, suggesting a degree of transformation. Nine patients were treated with DCF: one had complete resolution, six responded with 50-90% reduction of the lymphadenopathy, one did not respond and one is still on treatment; alpha-IFN was used concomitantly or sequentially in two of the responders. One responding patient died of sepsis after four injections of DCF. Three patients received either alpha- or beta-IFN alone with no response. One elderly patient was not treated. Abdominal lymphadenopathy could be part of the natural history of HCL and/or may represent a transformation analogous to that seen in other low-grade lymphoproliferative disorders. Routine abdominal CT scanning should be part of the work up of all patients with HCL.

Leucocyte suspension viscosity was measured using cells from a number of leukaemias. Samples from individuals with acute myelomonocytic and myeloid leukaemias, and chronic myelogenous and chronic lymphatic leukaemias were examined for their viscosity and flow properties. Leucocytes were suspended in native plasma and the effect of variable leucocyte numbers in the ranges seen in some leukaemias (100-600 x 10(9)/l) examined at different shear stresses. The effect of MCV was also determined in relation to viscosity. The results showed an increasing order of viscosity from the leucocytes of chronic lymphatic leukaemia through chronic myelogenous and acute myeloid leukaemia to the acute myelomonocytic variety. This bears some relation to the mean corpuscular volume, but confirms the fact that at high numbers of cells, patients with acute myelomonocytic, and to a lesser extent the myeloid leukaemias, are at considerable risk of blood hyperviscosity.

Transfusing allogenic blood still carries risks despite better screening of donors and improvements in typing, cross matching, and labelling of blood. Although blood is tested for HIV antibodies, time may elapse before infected blood tests positive.' 2 Transfused blood may disturb the recipient's immune system, affecting the growth of primary and secondary tumours35 and the development of graft versus host disease.6 The risk of clerical error or confusion over names is ever present and can result in patients receiving the wrong blood. One way ofreducing the risks of allogenic blood transfusion is to reduce the amount of allogenic blood that is transfused. Several methods exist for doing this. They include raising the threshold for perioperative transfusion, using the patient's own blood (obtained either preoperatively or by salvage), and using haemostatic drugs. The National Institutes of Health's consensus conference on perioperative red cell transfusion concluded that a haemoglobin concentration of 100 g/l or its equivalent (for example, a packed cell volume of 30%) need no longer be an essential requirement for surgery.' It stated that moderate anaemia did not contribute to perioperative morbidity, quoting the work of Carson et al, which suggested that a haemoglobin concentration of 80 g/l should be adequate.9 Applying such standards before operation would presumably reduce overall blood usage, but its acceptance by anaesthetists and surgeons might depend on further studies showing no adverse effect on postoperative morbidity and length of hospital stay. Messmer has shown that haemodilution to a packed cell volume of about 30% is well tolerated during surgery and states that "blood fluidity" and "nutritional blood flow" may even be enhanced. `Baron et al reported that similar levels of packed cell volume are also well tolerated in surgical patients, including those with coronary heart disease."' Total blood volume needs maintaining, and arterial oxygen saturation must be adequate. Normovolaemic haemodilution could be achieved immediately before surgery by removing 600-1000 ml of whole blood and replacing it with a suitable plasma expander. The blood could then be returned to the donor. As this procedure is carried out at the time of surgery the chances of administrative error are minimised. Its drawback is that it is yet another process to be undertaken perioperatively, requiring additional resources of labour and materials. The use of predonated autologous blood by patients requiring blood for planned operations has attracted considerable interest recently. The human bone marrow responds very well to a reduction in red cell mass: if iron supplements are given then removing up to four units of blood may be possible before surgery while still preserving an acceptable preoperative haemoglobin concentration. This blood would then be available for transfusion during surgery. Blood predeposit and predonation programmes have been publicised in the United States,' Italy,'" Belgium," and the United Kingdom.'4 This technique sidesteps the problems of infection or immune disturbance and leaves only the risk of clerical error. Its logistics, however, are formidable. Firstly, the donated blood needs handling with the same technical and administrative skill that allogenic donated blood does. To protect staff who come in contact with it autologous blood needs screening for the same infectious agents as does allogenic blood (and donors should be informed of this policy). Secondly, as its use needs careful planning, the date of operation should be fixedruling out the procedure for many in Britain. Thirdly, the administrative effort of ensuring it arrives in the correct place at the correct time is considerable. In Britain, regional blood centres rather than local hospital centres dominate blood donations and trans fusions, which may have restricted the widespread use of autologous blood. The fact that there are no immediate cost savingsthe blood has to be processed in virtually the same way as any other unit of blood-doesn't recommend it on budgetary grounds. In the United States public demand has led to its increased use. In Frankfurt, where the Red Cross has been providing the service since 1974, autologous blood has never made up more than one third of all blood used and currently comprises about one fifth-despite the publicity given to the risks of AIDS.'9 Recent reports suggest that the antiprotease aprotinin is valuable in reducing bleeding and blood requirements in vascular surgery and thrombocytopenia (p 660). 621'' The search for artificial blood substitutes continues: some agents are currently being evaluated, but only in specialised centres so far. Several devices for intraoperative blood salvage have been marketed: these collect blood that is shed during operation and return it to the patient, with or without washing. No formal comparisons have been made among the various systems, which seem safe and useful. Reducing the amount of allogenic blood that is transfused by these methods may require extra effort, but relying more

Factor X-activating activity (FXAA) was determined by a chromogneic assay in normal and malignant breast tissue. FXAA was found in all tissue (n = 38) irrespective of pathology, and the activity of normal tissue was similar to that of tumours. FXAA correlated with tissue hemoglobin in normal breast (p < 0.02) but not in tumours. FXAA was markedly reduced by aluminium hydroxide, barium citrate, anti-human factor VII, DFP, PMSF and phospholipase C, but was unaffected by iodoacetamide and mercuric chloride. It is concluded that FXAA is a serine protease with the properties of a tissue factor-factor VII complex. FXAA occurs in normal and malignant breast tissue, although the 'normal' activity may be an artefact of the homogenization process.

Whole blood procoagulant activity was determined by measuring the endotoxin-induced shortening of the celite-activated whole blood recalcification time in patients with breast cancer (n = 29), colorectal cancer (n = 18), benign breast disease (n = 26), benign colorectal disease (n = 10), normal volunteers (n = 17) and surgical in-patients with non-malignant and non-inflammatory conditions (n = 18). Using this method, patients with breast and colorectal cancer produced significantly more procoagulant activity than normal controls (P less than 0.001), surgical in-patients (P less than 0.005) and patients with benign breast (P less than 0.001) and benign colorectal (P = 0.05) disease respectively. The difference between subjects classified as 'cancer' or 'non-cancer' was highly significant (P less than 0.0001). There were no significant differences in total white cell or absolute monocyte counts between subject groups, and in individual patients, there was no correlation between these parameters and the procoagulant activity. It is concluded that the activated whole blood recalcification time is a more reproducible way of measuring whole blood procoagulant activity than the original technique, and that using this method, patients with cancer show higher procoagulant activity than corresponding benign controls.

Whole blood procoagulant activity was determined by measuring the recalcification time of citrated blood, with and without the addition of bacterial endotoxin, in patients with breast cancer (n = 39), colorectal cancer (n = 20), benign breast disease (n = 15), benign colorectal disease (n = 11), normal volunteers (n = 15) and inpatients with non-malignant disease (n = 22). The median clotting times of those samples incubated with endotoxin were significantly shorter in the patients with breast and colorectal cancer compared with normal controls. Furthermore, significant differences between the median clotting times of stimulated and unstimulated samples within each subject group were observed only in the two cancer groups. There was no correlation between whole blood procoagulant activity and absolute monocyte counts, with histological staging or with plasma concentrations of plasma fibrinopeptide A. The results suggest that blood from patients with cancer is more sensitive to endotoxin stimulation than that from normal or benign controls, but that in its present form the technique cannot be used to distinguish between malignant and non-malignant disease.

The Journal of PathologyVolume 155, Issue 1 p. 91-92 Book Review The acute leukaemias. Biologic, diagnostic and therapeutic determinants. S. A. Stass (Ed.). Marcel Dekker, New York, 1987. No. of pages: 496. Price $138.00.ISBN: 0 8247 7766 2 S. Roath, S. Roath University of SouthamptonSearch for more papers by this author S. Roath, S. Roath University of SouthamptonSearch for more papers by this author First published: May 1988 https://doi.org/10.1002/path.1711550115AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume155, Issue1May 1988Pages 91-92 RelatedInformation

Transient acquired B red cell antigen was found in a patient with inflammatory bowel disease. Removal of the affected portion of the bowel was associated with disappearance of the B antigen. This phenomenon has usually been recorded in association with neoplasms of the bowel, but appears to be a marker for the release of bacterial enzymes into the systemic circulation associated with breakdown of the normal bowel barrier to such materials.

Conference Abstract| September 01 1983 The Influence of Age and Sex on Whole Blood Viscosity R. Warrell; R. Warrell 1Departments of Geriatric Medicine and Haematology, University of Southampton Search for other works by this author on: This Site PubMed Google Scholar G. Adkins; G. Adkins 1Departments of Geriatric Medicine and Haematology, University of Southampton Search for other works by this author on: This Site PubMed Google Scholar A. Abdullah; A. Abdullah 1Departments of Geriatric Medicine and Haematology, University of Southampton Search for other works by this author on: This Site PubMed Google Scholar R.S. Briggs; R.S. Briggs 1Departments of Geriatric Medicine and Haematology, University of Southampton Search for other works by this author on: This Site PubMed Google Scholar P. Davenport; P. Davenport 1Departments of Geriatric Medicine and Haematology, University of Southampton Search for other works by this author on: This Site PubMed Google Scholar S. Roath S. Roath 1Departments of Geriatric Medicine and Haematology, University of Southampton Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1983) 65 (3): 13P–14P. https://doi.org/10.1042/cs065013Pb Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation R. Warrell, G. Adkins, A. Abdullah, R.S. Briggs, P. Davenport, S. Roath; The Influence of Age and Sex on Whole Blood Viscosity. Clin Sci (Lond) 1 September 1983; 65 (3): 13P–14P. doi: https://doi.org/10.1042/cs065013Pb Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu nav search search input Search input auto suggest search filter All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1983 The Biochemical Society and the Medical Research Society1983 Article PDF first page preview Close Modal You do not currently have access to this content.

Ten individuals with idiopathic neutropenia and similar numbers of normal and abnormal controls were tested for mobilization of their marginal granulocyte pools and bone marrow reserve by using epinephrine and hydrocortisone intravenously. Individuals with 'benign' idiopathic neutropenia appeared to have a normal response while half the abnormal controls responded poorly. It is suggested that granulocyte mobilization tests are valuable in the assessment of individuals with neutropenia.

Histamine release and changes in cyclic AMP levels induced by a variety of stimuli have been measured in isolated human leucocytes from a patient with 40-70% basophilia. Adenosine and sodium fluoride induced early monophasic rises in cyclic AMP which peaked at 1 min, but they did not release histamine. 2',5'-Dideoxyadenosine (DDA) caused a transient fall in cyclic AMP levels. Anti-IgE, polylysine and calcium ionophore A23187 induced a slow release of histamine commencing 2-5 min after addition of secretagogue. With polylysine and A23187, release was still proceeding 45 min after challenge. In contrast, the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (f-met-leu-phe) induced a rapid secretion of histamine which was complete within 2 min. Anti-IgE induced a rapid monophasic rise in cyclic AMP which reached a maximum at 45 sec and was inhibited by pretreatment with DDA. Cyclic AMP rises induced by polylysine and f-met-leu-phe were kinetically similar but smaller in magnitude. A23187 caused a later rise in cyclic AMP which peaked 3 min after challenge. A high concentration (50 microM) of compound 48/80 induced a slow cytotoxic release of histamine which was not accompanied by changes in cyclic AMP levels. The inconsistent quantitative and kinetic relationships of histamine release and cyclic AMP production suggest that changes in cyclic AMP levels may not play a key role in the biochemical events leading to mediator secretion from human basophil leucocytes.

The sera of 74 individuals with chronic lymphoproliferative disease were screened for the presence of inhibitory activity against neutrophil chemotaxis. This was present in more than half the patients with IgA myeloma and Hodgkin's disease but was less common in chronic lymphocytic leukaemia, lymphocytic lymphoma and non-IgA paraproteinaemia. Heating the sera prior to testing frequently enhanced inhibitory activity particularly in myeloma and lymphoma.