CORRESPONDENCE Angiogenesis and mast cells in Hodgkin lymphoma

Hodgkin lymphoma (HL) differs from other lymphomas because the malignant cells, the Hodgkin and Reed–Sternberg (HRS) cells, are in minority and the majority of the tissue consists of surrounding benign cells, for example, eosinophilic granulocytes and mast cells, fibrosis and a varying number of microvessels. It has recently been reported that angiogenesis correlates to poor prognosis in HL. We have previously reported that HL patients with many mast cells in their tumour tissue have a worse prognosis. Mast cells produce functionally active CD30 ligand (CD30L) and the poorer prognosis has been proposed to be caused by a stimulation of HRS by CD30L. Furthermore, we have shown that mast cells, upon stimulation with CD30, release cytokines and chemokines, among which interleukin-8 (IL-8) is known to have angiogenic properties (manuscript in preparation). In other lymphomas, mast cells are proposed to contribute to angiogenesis. In order to increase our understanding of inflammatory cells, their importance in tumour progression and especially angiogenesis in HL, we investigated the possible relation between the number of mast cells and the microvessel count in primary diagnostic HL tissue. We also wanted to further elucidate the prognostic implication of microvessel count in HL. Patient samples and clinical data were acquired from the database of the National Health Care Programme for HL in Sweden. A total of 120 patients treated with curative intention, according to the principles of the Health Care Programme in the Uppsala/Örebro health care region between 1989 and 1994, were included. The paraffin-embedded tissue samples were from HL involved lymph nodes from the primary diagnosis. The clinical characteristics are presented in Table 1. Progression free survival (PFS) and HL specific survival (HLS) were analysed. The mean follow-up of living patients was 11 years (range 6–15 years). The estimation of the number of microvessels immunohistochemically stained for CD31 (Figure 1), was done by one of the authors using the Chalkley technique. Three to five fields with the highest concentration of vessels (a hot spot) were counted and an average of the highest three countings in every case was used. In all, 20 cases were recounted independently by another author and the counts correlated with an R-value of 0.75, (P1⁄4 0.0002). All evaluations were done without knowledge of patient data. The counts varied from 1 to 12 vessels/hot spot. The median was 3 and the 75th percentile was 4.3 vessels/hot spot. Nonbulky disease correlated to high microvessel count