Search

Between 1 January 1980 and 31 July 1988, 62 patients with chronic lymphocytic leukaemia (CLL) or malignant non-Hodgkin's lymphoma (NHL) were splenectomized for splenomegaly and presumed hypersplenism. All patients except one had splenomegaly (mean(s.d.) weight 1585 (872) g, range 150–4300 g) and 34 had massive splenomegaly (> 1500 g). Forty-nine patients had platelet counts < 100 × 109/l and 16 patients had anaemia with haemoglobin levels < 10 g/dl. White cell counts were < 3×109/l in six NHL patients. Fifteen patients had bicytopenia, and three NHL patients had tricytopenia. The selected group of 62 patients underwent splenectomy largely because of failure to respond to medical therapy (39 patients) or inability to tolerate or start adequate chemotherapy because of very low blood counts (11 patients). There was one postoperative death, and a 29 per cent morbidity rate. The response rate was 89 per cent in the first month after splenectomy and 39 patients (63 per cent) had a continuing complete response with a median follow-up of 26 months (range 3–96 months). Twelve patients (10 with CLL) received no further therapy after splenectomy. Seven patients failed to respond and 15 relapsed after splenectomy. These 22 patients could be distinguished on the basis of: (1) lower average preoperative platelet counts (P < 0·007), postoperative platelet counts (P < 0·001), and postoperative rise in platelets (P < 0·004); (2) lower average spleen weight (P < 0·052); (3) preoperative chemotherapy (P < 0·044). However preoperative and postoperative platelet counts were the only two variables selected by stepwise regression analysis (P < 0·05 and P < 0·01, respectively). Bone marrow failure did not preclude complete response after splenectomy. Long-term survivors emerged from the group of patients with continuing complete response. Of the seven patients who failed to respond, five died with a median survival of 4 months, and of the 15 patients who relapsed after splenectomy, 13 died, with a median survival of 6 months after relapse and 18 months after splenectomy. Thus, splenectomy may be an effective palliation for both CLL and NHL patients with splenomegaly and hypersplenism.

Resume Les complications neurologiques sont frequentes au cours des infections par le retrovirus HIV et notamment au cours du SIDA. Elles semblent, d'apres la litterature, concerner plus souvent le systeme nerveux central (SNC) que peripherique (SNP). Une etude prospective a ete realisee pour tenter d'apprecier la frequence et le type des atteintes du SNP au cours des infections par le HIV dont le neurotropisme est maintenant bien etabli. Quarante et un patients infectes par le HIV (5 porteurs asymptomatiques, 14 SAS [ou ARC] et 22 SIDA) ont ete etudies sur les plans clinique et biologique; 40 ont egalement eu une etude EMG et des vitesses de conduction nerveuse. Vingt-six ont eu une PL et 25 une biopsie nerveuse (associee 3 fois a une biopsie musculaire). Il ressort de cette etude que l'existence d'une alteration du SNP est extremement frequente (36/41, soit 88% des cas), le plus souvent moderee, voire infraclinique (17/36); elle prend le plus souvent l'aspect d'une polyneuropathie sensitive axonale. Des neuropathies de caractere plus severe (polyradiculonevrite, polyneuropathie sensitivo-motrice, etc.) sont egalement possibles mais beaucoup plus rares. Enfin, quelle que soit sa forme, l'atteinte du SNP peut s'observer chez les sujets dits porteurs asymptomatiques (2/5) aussi bien que chez les SAS (12/14) et chez les SIDA (22/22). Elle temoigne soit d'une atteinte directe du nerf par le HIV, soit de mecanismes immuns (a mediation humorale et/ou cellulaire), soit de l'association des deux mecanismes.

Various procedures for immunoprotection in the A-SW mouse SEWA tumour system were compared. Four types of protector agents were used: polyoma virus, allogeneic S724 cells, A9/SEWA hybrid cells and xenogeneic ST(py) cells. Several injection schedules were also employed. On the whole, reasonable immunoprotection was obtained. The results, when allogeneic hybrid or xenogeneic cells were used, were comparable with those obtained for polyoma virus. This indicates that the T.A.T.A. of the SEWA tumour had been well conserved. When polyoma virus alone was used as the protector agent, injection 7 days before the tumour challenge, or iterative injection, afforded better protection than a single injection on the day of challenge.

Good immunoprotection was afforded by A9/SEWA somatic hybrid cells in the C3H mouse/C3H Py tumour system, confirming results previously obtained in the A.SW mouse/SEWA tumour system. However, in this study the immunogenicity decreased with increasing serial subculture of the hybrid line and concomitant chromosome loss.

It now seems possible to predict response to anti-cancer drugs by means of several methods classified into three groups. Methods in the first group are aimed at determining the intracellular mechanisms required for the drugs to act on the tumoral cells; apart from hormone receptor assays, few of these have practical applications. Methods in the second group are concerned with the action of cytostatic drugs on malignant cells; clonogenic cultures and human tumour xenografts in mice are already routinely used. Finally, methods to evaluate the pharmacokinetics of anticancer drugs are being developed. These three groups of methods can be used in the pre-clinical screening of these drugs or at the clinical trial phase to predict individual responses to chemotherapy.