99mTc-labelled glucosamine in the assessment of systemic sclerosis inflammatory lung disease: a novel inexpensive investigative tool with predictive value.

Objective To evaluate the role of Tc-99m-labelled glucosamine [Tc-99m-ECDG] as a clinical biomarker for the early detection of interstitial lung disease (ILD) in systemic sclerosis (SSc). Methods In this prospective pilot study, glucosamine scanning (GS) was performed in 15 SSc patients, with and without ILD. Collected data included patient disease characteristics, autoantibody profile, GS results, high-resolution computerised tomography [HRCT], pulmonary function tests [PFT], and transthoracic echocardiogram [TTE]. Glucosamine results were correlated with patient clinical profile, HRCT, and PFT's findings. Results Lung uptake of Tc-99m-ECDG was high in 4 patients, moderate in 3, mild in 5, and normal in 3 with SSc, respectively. Of the patients with high and moderate uptake there was a 100% correlation between Tc-99m-ECDG uptake and HRCT showing ILD. Of the 5 patients with mild Tc-99m-ECDG uptake, 4 patients had aspiration pneumonia, and 1 had early ILD using HRCT. Of the 3 patients with normal Tc-99m-ECDG, 2 had normal HRCTs; the third had severe pulmonary arterial hypertension with minimal HRCT changes of ILD. High and moderate Tc-99m-ECDG lung uptake predicted abnormal PFT's in 100% of cases. In 3 patients, there was less extensive disease depicted on the Tc-99m-ECDG scans than on the HRCT. These patients demonstrated a more favourable outcome than would have been expected from the HRCT scans alone. Mild Tc-99m-ECDG lung uptake correlated with abnormal PFT's in 60% of cases. The pattern of Tc-99m-ECDG uptake was excellent (100%) at distinguishing metabolically active ILD from aspiration pneumonia. Diffuse uptake was noted in the former and patchy uptake in the latter disease entity. Conclusion Increased Tc-99m-ECDG uptake in scleroderma lung correlated positively with both structural and functional changes. Tc-99m-ECDG is a useful adjunct helping elucidate inflammation secondary to aspiration pneumonia and/or other causes of abnormal PFT's.