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In a retrospective study, we used a series of 29 patients with Sjögren's Syndrome diagnosed according to the new European criteria (Cl. Vitali, S. Bombardieri, H. M. Moutsopoulos et al.) (8). (Arthritis Rheum 1993; 36:340-7). A labial biopsy technique allowed to classify these patients into the anatomical "scores" formerly related by Chisholm and Mason and Chomette et al. Referring to these criteria, only 45% of patients presented a characteristic histopathological pattern. If another complementary criterium, i.e. ductal tropism of lymphoid infiltrates, was added, that percentage remained low (50% only). Thus, these results would suggest the following considerations: the classical histopathological criteria do not seem sufficiently specific; other histological criteria such as ductal lesions previously noted by Leroy et al. must in addition be looked for; thus it would seem to be of considerable value to use in the future complementary quantitative studies by means of morphometric methods.

Cystic lymphoid hyperplasia of the parotid, a rare disease, was recently described in patients with acquired immunodeficiency syndrome. We reported here 2 new cases of this illness. The 2 HIV+ patients showed an enlargement of parotid gland. A superficial parotidectomy was performed. The histological and immunohistochemical studies were completed in one case by a histoenzymological and ultrastructural study. We could see numerous cystic cavities lined with a cylindrical or metaplastic malpighian epithelium and surrounded by a lymphoid tissue, similar to a true lymph node with germinal centers. In these lymphoid structures, we could find some epithelial remnants and numerous epimyoepithelial islands. Besides, anomalies similar to those described in persistent generalized lymphadenopathies were obvious: hyperplastic germinal centers with multiplication of B lymphocytes and thin mantle zone, perifollicular hypervascularization, numerous macrophages, plasmocytes and T lymphocytes with increase of T8 cytotoxic subset in interfollicular and paracortical areas. An early opportunist infection is suggested in the histogenesis of this disease.