Expérimentalement, une carence en acides gras essentiels (acides gras non synthétisés par l’organisme), entraîne l’atrophie de la glande lacrymale. Il en est de même en cas de carence en pyridoxine (Vitamine B6).
Chez l’homme, une carence en Vitamine C favorise l’apparition du syndrome de Gougerot-Sjögren.
Tous ces éléments, acides gras essentiels, Vitamines B6 et C semblent donc indispensables à une bonne sécrétion lacrymale.

Ces 3 éléments ont un point commun : ils participent à la synthèse des PGE1, en fournissant l’acide cis-linoléique et l’acide gamma-linolénique (précurseurs), les Vitamines en favorisent les transformations métaboliques.

Il a été ainsi successivement démontré que :

  1. L’administration de PGE1 permet, chez la souris NZB/W (modèle animal du syndrome de Gougerot-Sjögren) d’augmenter considérablement la production lacrymale et salivaire.
    Sjogren’s syndrome and the sicca syndrome: the role of prostaglandin E1 deficiency.
    Treatment with essential fatty acids and vitamin C.
    Horrobin DF, Campbell A
    Med Hypotheses 1980 Mar;6(3):225-32
    PGE1 treatment has been shown to correct the immunological abnormalities in the NZB/W mouse, the animal model of Sjogren’s syndrome.
  2. De toutes les prostaglandines testées chez le lapin, seules les PGE1 ont permis de stimuler directement les glandes lacrymales.
    Secretory effect of prostaglandins on the rabbit lacrimal gland in vivo.
    Pholpramool C
    Prostaglandins Med 1979 Sep;3(3):185-92.
    Fluid secretion from the cannulated excretory duct of the rabbit lacrimal gland was collected in microcapillary pipette at 10 min intervals. Secretion rate and electrolyte concentrations (Na+, K+ and Cl-) in the lacrimal fluid samples were determined before and after injections of small doses of prostaglandins (PGE1, PGE2, PGF1 alpha, PGF2 alpha, 15 epi-PGF2 alpha, PGF2 beta, PGA1 & PGA2) into the external maxillary artery. Only PGE1 had a dose-dependent stimulatory effect on the lacrimal gland secretion. The maximum secretion rate which was induced by PGE1 (25 micrograms/kg) was 7.2 +/- 0.9 microliters/10 min. Na+ concentration in the fluid secretion stimulated by PGE1 was increased; however, K+ and Cl- concentrations were not changed. Pretreatment with atropine (50 micrograms/kg, I.A.) failed to prevent the stimulatory effect of low doses of PGE1. On the other hand, the secretory responses were abolished when propanolol (3 mg/kg, I.A.) was administered prior to PGE1. The results suggest that fluid secretion of the rabbit lacrimal gland in response to PGE1 may be caused by excitation of the sympathetic ganglia and/or by direct action on beta-receptors in the acinar cells.
  3. Une supplémentation alimentaire en huile d’onagre, Vitamine B6 et Vitamine C permet d’augmenter la quantité de larmes produites par l’organisme.
    Sjogren’s syndrome and the sicca syndrome: the role of prostaglandin E1 deficiency.
    Treatment with essential fatty acids and vitamin C.
    Horrobin DF, Campbell A
    Med Hypotheses 1980 Mar;6(3):225-32
    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. 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.
    Essential fatty acid and prostaglandin metabolism in Sjogren’s syndrome,
    systemic sclerosis and rheumatoid arthritis.
    Horrobin DF
    Scand J Rheumatol Suppl 1986;61:242-5
    Evidence from biochemical studies and from experimental animals indicates that abnormalities of essential fatty acid (EFA) and eicosanoid metabolism could lead to salivary and lacrimal gland atrophy and to immunological and cardio-vascular defects. Measurements of EFA levels in erythrocytes from patients with primary Sjogren’s syndrome have shown that abnormalities are indeed present. Controlled clinical trials of supplementation with gamma-linolenic acid (GLA) as evening primrose oil in both primary Sjogren’s syndrome and systemic sclerosis have given positive results. There are strong arguments to indicate that sophisticated manipulation of EFA metabolism may have a role to play, not only in Sjogren’s syndrome but also in other rheumatological disorders.
  • L’ASSOCIATION HUILE D’ONAGRE + VITAMINE B6 + VITAMINE C EST LA PLUS PERFORMANTE POUR STIMULER LA PRODUCTION DE PGE1 ENDOGÈNES
    The regulation of prostaglandin E1 formation:
    a candidate for one of the fundamental mechanisms involved in the actions of vitamin C.
    Horrobin DF, Oka M, Manku MS
    Med Hypotheses 1979 Aug;5(8):849-58
    Vitamin C stimulates the formation of PGE1 in human platelets. The effect occurs over the physiologically relevant range of concentrations. PGE1 is required for T lymphocyte function and plays a major part in the regulation of immune responses. PGE1 is also important in the regulation of collagen and ground substance metabolism, in cholesterol metabolism and in regulation of responsiveness to insulin. It is proposed that defective formation of PGE1 could account for many of the features of scurvy and for many of the reported therapeutic effects of vitamin C. If correct, vitamin C will be of value only in conjunction with an adequate supply of dihomogammalinolenic acid, the precursor of PGE1. Essential fatty acids, pyridoxine and zinc are all required to achieve this.