SUMMARYThe pathogenesis of avascular necrosis of bone (ANB) was investigated in 111 patients with systemic lupus erythematosus (SLE) (24 with ANB, 87 without ANB); patients' ages, corticosteroid treatment, clinical and laboratory features associated with SLE, and haemostatic profiles were all taken into account. The mean ages of patients with and without ANB at the time of diagnosis of SLE was 24-1 and 31*2 years respectively. The mean maximal daily dose of prednisolone in the group with ANB was 50*8 mg, which was significantly higher than the dose (41*8 mg) in the group without ANB. Disease features of SLE, such as Raynaud's phenomenon, hyperlipidaemia, nephrotic syndrome, hypertension, and disease activity, were not found to be related to ANB. The percentage of patients who had lupus anticoagulant as well as a shorter activated partial thromboplastin time was greater in those with ANB than in those without. Multiple factors may be involved in the pathogenesis of ANB in SLE, and it is suggested that haemostatic abnormalities, which could be influenced by corticosteroids and young ages, play some part in the development of ANB.Since 1960 when Dubois and Cozen suggested an association of avascular necrosis of bone (ANB) with systemic lupus erythematosus (SLE),1 ANB has continued to be one of the major problems during the course of SLE. Corticosteroids, which are used for most patients with SLE, have been implicated as one cause of ANB, 6 but multiple factors, such as vasculitis,7 8 fat emboli,9 10 Raynaud's phenomenon,6 11 and young ages,12 13 must contribute to its development. As ANB may result from interference with the blood supply,7 haemostatic abnormalities and factors which induce them could also contribute to its occurrence.In this study we attempted to determine the predisposing factors for ANB in SLE, considering particularly patients' ages, corticosteroid treatment, and haemostatic state.

The clinical importance of IgG anticardiolipin antibodies was investigated in systemic lupus erythematosus (SLE) in PBS 50 ,ul of serum which were to be tested (diluted to 1/50 with PBS containing 0-05% Tween-20 and 10% FCS) were added to each well and incubated for two hours at room temperature. After five washes with PBS 100 1d of alkaline phosphatase-labelled mouse monoclonal antihuman IgG (Miles, Naperville, Illinois, USA) was added to each well, and the plate was incubated for one hour at room temperature, followed by the addition of 100 RI of p-nitrophenyl phosphate (Sigma) in 1 M diethanolamine buffer (pH 9-8). After incubation for 30 minutes the optical absorbance was measured at 405 nm by Easy Reader (Laboscience, Tokyo, Japan). The values of IgG anticardiolipin antibodies were expressed as units compared with those of the standard serum. A positive result indicated a value in units more than 3 SD over the mean value obtained with control sera (106 healthy volunteers).

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To examine the mechanism of induction of differentiation in the human malignant T-lymphoblastic cell line, MOLT-3, by 12-O-tetradecanoylphorbol-13-acetate (TPA), the role of receptors for phorbol esters was investigated. Binding of [20–³H]-phorbol-12,13-dibutyrate to TPA-resistant subclones derived from MOLT-3 was less than50 % of that of the parental MOLT-3. Scatchard analysis showed that the concentration of phorbol ester receptors in a TPA-resistant subclone was about 50% of that in the parental MOLT-3, but affinities of binding were similar, indicating that more than a certain number of phorbol ester receptors is required to induce differentiation by TPA in this human T cell line.