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City Road, London EC] V2PD SUMMARY A control trial is reported which demonstrates that treatment with argon laser photocoagulation to certain patients with macular oedema following a branch vein occlusion does not alter significantly their visual prognosis. It confirms that patients with an intact perifoveal capillary arcade have a better prognosis than those with a broken arcade.

SUMMARYMicrovascular complications of insulin-dependent diabetes mellitus (IDDM) have been strongly associated with platelet abnormalities, whilst TNF-a has been implicated in the pathogenesis of this condition. However, at present it is not clear whether human circulating platelets express TNF-a or TNF receptors (TNF-R) or whether impaired expression of these molecules and of the TNF-reactive adhesion molecule ICAM-1 may be associated with platelet abnormalities in patients with IDDM. On this basis we investigated the platelet expression of these molecules in patients with IDDM complicated or uncomplicated by proliferative diabetic retinopathy (PDR) and in healthy subjects. We observed that the proportion of platelets staining for TNF-a was significantly higher in IDDM patients with active PDR than in patients without microvascular complications (P ¼ 0·0078), quiescent PDR (P ¼ 0·003) or healthy subjects (P ¼ 0·0013). Patients with active PDR also showed a higher proportion of platelets expressing TNF-RI (P ¼ 0·0052) and TNF-RII (P ¼ 0·015) than healthy controls or patients with quiescent PDR (P ¼ 0·009 and 0·0006, respectively). In addition, the percentage of ICAM-1 þ platelets was significantly higher in patients with active PDR than in patients with quiescent PDR (P ¼ 0·0065) or normal subjects (P ¼ 0·013). There was a direct correlation between platelet expression of TNF-a and that of TNF-R in PDR patients, indicating that platelet staining for TNF-a may be due to binding of this cytokine to its receptors. The results suggest that increased platelet expression of TNF-a, TNF-R and ICAM-1 in IDDM patients may constitute important markers of thrombocyte abnormalities during the development of microvascular complications of diabetes mellitus.

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TNF-alpha has been implicated in the pathogenesis of insulin- dependent diabetes mellitus (IDDM). At present there are no studies linking serum levels of soluble TNF receptors (sTNF-R) to the development of diabetic microvascular complications such as proliferative diabetic retinopathy (PDR), or to the production of TNF-alpha in these patients. We investigated serum levels of sTNF receptors (sTNF-RI and sTNF-RII) in IDDM patients with or without PDR, and related these to the in vitro production of TNF-alpha upon activation of whole blood and isolated mononuclear cells (MNC). We observed higher serum levels of sTNF-RI in IDDM patients with active (range 945-6630 pg/ml; P = 0.029) or quiescent PDR (range 1675-4970 pg/ml; P = 0.00092) than in individuals with IDDM without retinopathy (range 657-2617 pg/ml) or healthy controls (range 710-1819 pg/ml; P = 0.0092 and 0.0023, respectively). Increased serum levels of sTNF-RII were also seen in IDDM patients with active PDR (range 1749-5218 pg/ml; P = 0.034) or quiescent PDR (range 1494-5249 pg/ml; P = 0.0084) when compared with disease controls (range 1259-4210 pg/ml) or healthy subjects (range 1237-4283 pg/ml). Whole blood production of biologically active TNF-alpha was lower in PDR patients than in disease (P = 0.04) and healthy controls (P < 0.005), contrasting with a higher production of TNF-alpha by lipopolysaccharide (LPS)-activated MNC from PDR patients (P = 0.013). Inhibition of TNF-alpha by TNF-R in plasma supernatants of activated blood from PDR patients was demonstrated by increase of TNF-alpha activity in the presence of anti-TNF-RI and anti-TNF-RII antibodies. These observations suggest that abnormalities in TNF-alpha production and control may operate during the development of microvascular complications of diabetes mellitus.

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