A. M. Peters

Quantification of pulmonary uptake of indium-111 labelled granulocytes in inflammatory bowel disease

This study describes a method for quantifying the pulmonary trapping of indium-111 labelled polymorphonuclear (PMN) cells in patients with inflammatory bowel disease (1131) in comparison to non-inflamed controls. Twenty patients with extensive IBD were studied by 111In-PMN scintigraphy. Gamma-camera images were obtained at 2.5–4 h (early) and 20–25 h (late) after the injection of autologous PMNs labelled in plasma with 111In-tropolonate. Local uptake in the chest, iliac bone marrow, spleen and liver was quantified as the counts per pixel per second per MBq of injected 111In for both early and late scans. Fourteen subjects without inflammatory disease were studied as controls. IBD patients showed significantly greater loss of splenic activity between early and late scans compared with controls (mean ± SD: −35.7% ± 16.6% versus −4.5% ± 6.1%, P < 0.001). There was no significant difference between control and IBD groups with respect to liver and bone marrow uptake on both early and late scans. Chest uptake was significantly higher in patients with 11313 on both early (6.4 ± 1.6 cps/MBq/pix) and late (5.6 ± 1.5cps/MBq/pix) scans, compared with the controls (4.8 ± 1.3 cps/MBq/pix, P < 0.005 and 3.4 ± 1.0 cps/MBq/pix, P < 0.001 respectively). The chest uptake in the control group on the late scans demonstrated a significant linear correlation with iliac uptake (y=0.23x + 0.41, r=0.87, n=14). Assuming in controls that there is no parenchymal uptake of 111In, this regression enables an estimate to be made, based on iliac counts, of the count rate from bone marrow in the chest wall. After subtraction of this from the total chest count rate, the true parenchymal uptake was derived, which averaged (2.86 ± 0.91) cps/MBq/pix in the IBD group compared to zero assumed in the control group. The higher lung 111In-PMN uptake on the early scans in IBD compared to controls is suggested to reflect a combination of increased margination, compared to controls, and early migration, whilst the excess 111In-PMN retention on late scans represents extravascular migration only. The bone marrow correction technique for quantification of pulmonary migration of 111In-PMNs should prove useful for the evaluation of PMN kinetics in disease.