Gastric studies in sjögren's syndrome.

In 1943 Henrik Sj6gren first described the syndrome which bears his name. It is generally recognized that the diagnosis can be made when any two of the following three features are present: xerostomia with or without salivary gland enlargement, keratoconjunctivitis sicca, and connective tissue disease, usually rheumatoid arthritis (Bunim, 1961; Bloch and Bunim, 1963). The xerostomia and keratoconjunctivitis sicca are due to reduced secretion by the salivary and lacrimal glands which are the seat of chronic inflammatory change. Impaired secretory function has been reported in many other sites, including the nose, pharynx, upper oesophagus, trachea and bronchi, vagina, skin, and pancreas (Gordon and Shanbrom, 1958; Fenster, Buchanan, Laster, and Bunim, 1964). Reduced gastric acid secretion in Sjdgren's syndrome has been reported by several workers (Lutman and Favata, 1946; Godtfredsen,1947; Behrman and Lee, 1950; Morgan and Raven, 1952; Gurling, 1953; MacLean and Robinson, 1954; Szanto, Farkas, and Gyulai, 1957; and Gordon and Shanbrom, 1958). The significance of these reports is uncertain since most are concerned with individual cases and augmented histamine stimulation was rarely used. Other workers have observed apparently normal gastric acid secretion and normal gastric histology has been reported (Ellman, Weber, and Goodier, 1951; Cardell and Gurling, 1954). However, Joske, Finckh, and Wood (1955) noted significant gastritis on histological examination of mucosal biopsies from five patients. In the present investigation, in a group of patients with Sj6gren's syndrome, gastric secretion, using augmented histamine stimulation, gastric mucosal histology, and gastric mucosal autoantibodies have been studied.