Horrobin D F, Campbell A
Med Hypotheses. 1980 Mar;6(3):225-32. doi: 10.1016/0306-9877(80)90120-6.
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.
前列腺素(PG)E1合成不足可能是干燥综合征的关键因素。PGE1对泪腺和唾液腺分泌以及T淋巴细胞功能很重要:因此,缺乏PGE1可能是干燥综合征和干燥综合征的主要特征的原因。PGE1也可能是许多通常与这些综合征相关的其他特征的原因。这些特征包括雷诺现象、肾功能异常以及维生素C缺乏引发该综合征。维生素C在PGE1生物合成中很重要。在干燥综合征的动物模型NZB/W小鼠中,PGE1治疗已被证明可纠正免疫异常。通过给予必需脂肪酸PGE1前体、吡哆醇和维生素C来提高内源性PGE1的产生,从而治疗干燥综合征患者的尝试成功提高了泪液和唾液的分泌率。