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1. Human leucocytes whose adenine nucleotide pool was prelabelled with [3H]adenine were investigated for their capacity to release adenosine and its metabolites and histamine when activated with the calcium ionophore A23187, antiimmunoglobulin E and the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (f-MLP). 2. Sixty-nine per cent of the 3H-label assimilated by the cells was incorporated into their adenine nucleotide pool in the ratio adenosine 5′-phosphate (AMP):adenosine 5′-pyrophosphate (ADP):adenosine 5′-triphosphate (ATP), 3:1:1. Spontaneous release of label from leucocytes plateaued at 5 min at 22.1 ± 4.2% of the total radiolabel incorporated and mainly consisted of hypoxanthine, inosine and adenosine. 3. Activation of cells with the calcium ionophore A23187 (1.0 μmol/l) caused a net increase in [3H]purine release above baseline of 27.9 ± 4.6% accompanied by a net basophil histamine release of 46.6 ± 9.4%. A23187 (1.0–3.0 μmol/l) caused a parallel concentration-dependent release of labelled purines and histamine. Purified mononuclear cells and granulocytes exhibited a similar ionophore-dependent capacity to release [3H]purines. 4. The distribution of label did not significantly differ between supernatants of activated and non-activated cells. Preincubation of cells with dipyridamole (10μmol/l) and erythro-9-(2-hydroxy-3)-nonyladenine (EHNA) (10μmol/l) to inhibit uptake and catabolism of adenosine respectively, produced an increase in adenosine at the expense of hypoxanthine recovered from the supernatant of both ionophore-stimulated and resting cells. 5. Activation of leucocytes with f-MLP (1.0μmol/l) caused a net increase in release of basophil histamine, but was associated with only a transient net increase in release of [3H]purine in four of five experiments. Immunoglobulin E-dependent stimulation produced basophil histamine release in the absence of detectable [3H]purine release. 6. These data demonstrate that leucocytes can be stimulated to release adenosine and related nucleoside matabolites accompanying the release of basophil-derived histamine. As adenosine is a bronchoconstrictor in asthma and leucocyte infiltration of the airways is a characteristic feature of the disease, leucocyte-derived adenosine may contribute to the pathogenesis of airways obstruction.

We report a case of plant thorn injury-induced tenosynovitis of the index finger of the left hand that was cured after surgical removal of the foreign body and partial synovectomy. We review current literature on this infrequently reported topic. Pathologically, thorn synovitis represents a foreign body reaction to retained plant material and is mostly aseptic. The presentation is delayed with the history of preceding injury often forgotten, and the diagnosis thus relies on careful elicitation of history. Imaging may be helpful to localize the plant material when the history is not clear. When possible, removal of the foreign material leads to complete remission, although some patients need partial or total synovectomy.