Modulation of neutrophil responses by adenosine may have an important role in limiting tissue injury during inflammation or ischemia-reperfusion. Mac-1 (CD11/CD18), a member of the leukocyte integrin family, participates in neutrophil adhesion to endothelium, in transendothelial migration, and in phagocytosis. Using monoclonal antibodies and flow cytometry, we investigated the effect of adenosine on the increase in plasma membrane expression of Mac-1 which occurs following stimulation of neutrophils with the chemotactic peptide N-formylmethionylleucylphenylalanine (FMLP). Adenosine and 5'N-ethylcarboxamido-adenosine, a potent A2 agonist, each produced a dose-dependent inhibition of as much as 50% of the increase in Mac-1 expression on neutrophils stimulated with FMLP, with an IC50 of approximately 1 nM. The effect of adenosine was blocked by 8-p-sulfophenyltheophylline, an adenosine-receptor antagonist, N6-cyclopentyl-adenosine, an A1-selective agonist, had no effect on FMLP-stimulated Mac-1 expression in the concentration range expected for its action on neutrophil adenosine receptors of the A1 type. We also found that dibutyryl cyclic adenosine monophosphate inhibited the upregulation of Mac-1, and that the effect of adenosine on Mac-1 expression was not reversed by colchicine or vinblastine. We conclude that adenosine acts via A2 receptors to inhibit the upregulation of Mac-1 expression of FMLP-stimulated neutrophils, and that A1 receptors are not involved. This effect of adenosine may help to limit Mac-1-dependent neutrophil exudation at sites of inflammation or ischemia-reperfusion.

A 49 year old woman with a four year history of rheumatoid arthritis had received aspirin 4 g/day and, for the past nine months, oral methotrexate 7 5-15 mg/week. Her blood counts were always normal during treatment. The patient presented with fever after dental extraction. The total white blood count was 1 1 x 109/1. Blood and urine cultures showed no growth and a chest radiograph was normal. She was admitted to hospital for four days and given intravenous penicillin and gentamicin. Three days later she was readmitted with a fever of 39 6°C, shortness of breath, and diarrhoea. The total white cell count was 3.5 x 109/1 (54% neutrophils, 1% band forms, 17% lymphocytes, 28% monocytes). A chest radiograph showed increased interstitial markings bilaterally, and a Grocott-Gomori methenamine silver nitrate stain of a transbronchial biopsy specimen showed P carinii. The patient required ventilatory support for nine days. She was treated with trimethoprim-sulphamethoxazole (20 mg/ 100 mg/kg a day) and later pentamidine (4 mg/kg a day), and was discharged after three weeks. She denied risk factors for human immunodeficiency virus infection, and the result of a test for antibody to the human immunodeficiency virus type 1 (HIV-1) by ELISA was negative. She has been treated with sulphasalazine, aspirin, and prednisone 5-10 mg/ day to control her symptoms of arthritis for 60 months since discharge, with no evidence of lung disease. PATIENT 3 A 64 year old woman with a 15 year history of rheumatoid arthritis had been treated for the past 30 months with sulindac 400 mg/day, prednisone 7 0 mg/day, and oral methotrexate 15 mg/week. Her blood count was always normal. She was admitted to hospital with weakness, chills, night sweats, dyspnoea, and cough. Her temperature was 39-4°C, and lung examination showed bilateral basal crackles.The total white cell count was 2-2 x 109/l (88% neutrophils, 2% band forms, 7% lymphocytes, 2% eosinophils, 1% basophils). The chest radiograph showed diffuse reticulonodular interstitial shadowing. GrocottGomori methenamine silver nitrate staining of bronchoalveolar lavage fluid showed P carinii. Despite ventilatory support and treatment

Diabetic ketoacidosis is traditionally stated as being capable of precipitating haemolysis in patients deficient in glucose-6-phosphate dehydrogenase (G6PD). This, however, is based on only a few case reports with inadequate documentation. A study was therefore conducted to review the subject in people with the Mediterranean variant of G6PD deficiency.Perusal of the medical records for the years 1970-82 yielded 15 patients with G6PD deficiency who had been

A case of late haematogenous pneumococcal infection of a prosthetic hip joint is presented. In view of the relatively benign nature of pneumococcal arthritis, the patient was treated with parenteral antibiotics and surgical drainage without removal of the prosthesis. This was followed by complete resolution.