Search

Six cases representing the spectrum of haematological complications due to systemic administration of Thorotrast are reposted. Two patients suffered from acute leukaemia, one patient had marrow failure and three patients presented with haematological features of hyposplenism; two of these also had solid tumours. The literature is reviewed.

Thirty-six (10.1 per cent) of a total of 355 adult patients with non-Hodgkin's lymphoma seen over a seven and a half year period developed compression or infiltration of the central nervous system (CNS). In nine patients (2.5 per cent) extradural tumour masses compressed the spinal cord or brain. Five of these patients, all previously untreated, responded well to treatment, with excellent recovery of CNS function and survival in the long term. The prognosis for the four patients with advancing drug-resistant systemic disease at the time of CNS compression was poor. In 27 patients (7.6 per cent) a clinical or cytological diagnosis of meningeal infiltration was made (on cerebrospinal fluid). Meningeal disease was seen most frequently in patients with high-grade lymphoma, either at presentation or during subsequent progression of systemic disease. All of these patients have died of systemic and/or CNS disease less than 20 (median 3) months from diagnosis of meningeal disease. Meningeal infiltration represents a significant clinical problem for which new approaches to prophylaxis and treatment are required.

Thirty-eight patients age 65 years and older with a diagnosis of non-Hodgkin's lymphoma of poor prognostic type were seen over a five and a half year period. These patients represented 19 per cent of our total new patient non-Hodgkin's lymphoma population during this time. Advanced age, coexisting medical illness, widespread lymphoma and poor treatment compliance were common problems. Despite this we were able to render 26 per cent of patients disease-free for periods from 12 to over 48 months. Age should not be considered a bar to staging and effective therapy. Palliative management was unsuccessful, and we believe that treatment should be given with the intention of cure. Features suggesting that a patient was more likely to achieve a lasting complete remission included early stage (I-IIA), a lack of systemic ('B') symptoms, an absence of bone marrow or bulky gastrointestinal tract disease and no pre-existing serious medical condition.

Complete or near complete remission of acquired pure red cell aplasia, not associated with thymoma, occurred in response to prednisone (six occasions), prednisone and cyclophosphamide (twice), cyclophosphamide alone (once) and splenectomy (once). These results were observed in four patients and confirm the value of cyclophosphamide and possibly splenectomy in patients resistant to prednisone in acquired red cell aplasia. In two of these patients, bone marrow progression from a state of ineffective erythropoiesis with many red cell precursors to that of red cell aplasia was observed. This indicates that some acquired refractory anaemias characterized by ineffective erythropoiesis may have the same pathogenesis as acquired red cell aplasia. The absence of demonstrable antibodies active against erythroblasts may merely reflect the insensitivity of currently available techniques. However it is possible that non-humoral immune mechanisms may be involved in the production of some forms of acquired red cell aplasia responsive to immunosuppressive drugs.