Annette Lake1, Iain J. Nixon2, Paula Beattie3, Kim Ah-See4, Dominic Culligan5, Nicholas Heaney6, Pam McKay6, Omar J. Hilmi7, Ruth F. Jarrett1
1 MRC-University of Glasgow Centre for Virus Research, Glasgow, UK, 2 NHS Lothian/Edinburgh University, Edinburgh, UK, 3 Royal Hospital for Children NHS Trust, Glasgow, UK, 4 Department of Otolaryngology-Head and Neck Surgery, Aberdeen Royal Infirmary, Aberdeen, UK, 5 Department of Haematology, Aberdeen Royal Infirmary, Aberdeen, UK, 6 Department of Haematology, Beatson West of Scotland Cancer Centre, Glasgow, UK, 7 Department of Otolaryngology, Head and Neck Surgery, Glasgow Royal Infirmary, UK
The vast majority of classical Hodgkin lymphoma (cHL) patients have raised serum and plasma CCL17 (TARC) levels at presentation. The aim of this study was to determine whether CCL17 testing could be used to speed up the diagnosis of cHL in young people presenting to their GP with lymphadenopathy. This study was prompted by the identification of a seemingly healthy member of our group with a raised CCL17 level. This led to hospital referral and diagnosis of cHL. Since raised serum CCL17 has also been associated with atopic dermatitis (AD), a secondary aim was to determine the range of levels in patients with AD. We also investigated the possibility of identifying cHL patients by measuring CCL17 in samples submitted for infectious mononucleosis (IM) testing.
This pre-planned interim analysis included serum CCL17 results from 58 patients presenting with lymphadenopathy (43 from neck lump clinics and 15 from haematology), and 10 patients referred to hospital with severe AD. All patients were aged 10–25 years. Surplus plasma was available from 500 samples submitted for IM testing. CCL17 levels were measured using the R&D Systems Quantikine ELISA. Pre-determined cut-off values of 1150 pg/ml and 850 pg/ml were used to define raised CCL17 in serum and plasma, respectively.
CCL17 levels in patients presenting with lymphadenopathy ranged from 77–135239 pg/ml. Two of the 43 neck lump clinic patients had raised CCL17; both were subsequently diagnosed with cHL while all of the patients with normal CCL17 levels had other conditions. All patients recruited through haematology had raised CCL17; 14 had a cHL diagnosis and the remaining patient had sarcoidosis, a disease previously associated with modest CCL17 elevation. CCL17 levels in AD patients ranged from 686–20276 pg/ml and 6 had levels above the cut-off. Levels were significantly lower in AD than cHL but the range of values overlapped. Among samples submitted for IM testing, 6 had raised CCL17 with marked elevation in 3 samples, raising suspicion of cHL.
These interim data suggest that CCL17 is a sensitive and specific biomarker for cHL, which has the potential to streamline the diagnosis of cHL in young people presenting with lymphadenopathy. The overlap of CCL17 values in cHL and AD suggests that it is important to exclude AD as the cause of a raised CCL17 level but this should be clinically straightforward. CCL17 testing at the same time as IM testing may lead to the early diagnosis of cHL in some cases.