Lack of adequate synthesis of prostaglandin (PG) E1 may be the key factor in Sjogren's syndrome.

PGE1 is important for lacrimal and salivary gland secretion and for T lymphocyte function: a deficiency could therefore account for the main features of Sjogren's syndrome and the sicca syndrome.

PGE1 could also account for many of the other features often associated with these syndromes. These include the Raynaud's phenomenon, the abnormalities of renal function and the precipitation of the syndrome by vitamin C deficiency. Vitamin C is important in PGE1 biosynthesis.

PGE1 treatment has been shown to correct the immunological abnormalities in the NZB/W mouse, the animal model of Sjogren's syndrome. An attempt to treat humans with Sjogren's syndrome by raising endogenous PGE1 production by administration of essential fatty acid PGE1 precursors, of pyridoxine and of vitamin C was successful in raising the rates of tear and saliva production.