No abstract

Abnormalities in plasma composition of essential fatty acids (EFAs) may be associated with the etiology of pruritus and other skin problems in patients undergoing hemodialysis. To study whether an oral supplementation with ω–6 (n–6) EFAs would restore deranged plasma EFAs and ameliorate skin symptoms, 9 and 7 dialysis patients were randomly assigned to receive either γ-linolenic acid (GLA)-rich evening primrose oil (EPO) or linoleic acid (LA) (2 g/day each) for 6 weeks. Plasma concentrations of EFA were analyzed by gas chromatography and uremic skin symptoms were assessed for dryness, pruritus and erythema by questionnaire and visual inspection in a double-blind manner. The patients given EPO exhibited a significant (p < 0.05) increase in plasma dihomo-γ-linolenic acid (a precursor of anti-inflammatory prostaglandin E₁) with no concomitant change in plasma arachidonic acid (a precursor of pro-inflammatory prostaglandin E₂ and leukotriene B₄). In contrast, those given LA exhibited a significant (p < 0.05) increase in LA but not in any other n–6 EFAs, whereas they exhibited a significant (p < 0.05) decrease in plasma docosahexaenoic acid. The patients given EPO showed a significant (p < 0.05) improvement in the skin scores for the three different uremic skin symptoms over the baseline values and a trend toward a greater improvement (0.05 < p < 0.1) in pruritus scores than those given LA. Results indicate that GLA-rich EPO would be a more favorable supplemental source than LA in terms of shifting eicosanoid metabolism toward a less inflammation status through modifying plasma concentrations of their precursor n–6 EFAs. Further studies are required to confirm the efficacy and safety of EPO therapy for the treatment of uremic pruritus.

These results suggest that 1) IL-1 effects depended on the dose, route and duration of administration, and 2) IL-1 enhances the responsiveness of rats to stressful environmental stimuli. In addition, the sub-chronic administration of IL-1 induces behavioral, neurotransmitter, hormonal and immune changes that may be causally implicated in the mechanism of some of psychiatric disorders such as depression.

SYNOPSIS A theory of migraine etiology should explain clinical features, biochemical correlates, and actions of effective therapies. Prostaglandin El (PGE1) involvement in migraine has been investigated, but the findings did not fulfill the above criteria. In the present study, low concentrations of PGE1 potentiated vasoconstriction, and increased PGE1 concentrations produced vasodilatation. Postaglandin synthesis in blood vessel walls was stimulated by prolactin, serotonin and angiotensin, explaining the assocation of migraine with sleep, stress, fluid and electrolyte retention, renal disease and dietary precipitating factors. Finally it was shown that propranolol, amitriptyline, caffeine and other drugs are prostaglandin (PG) antagonists, probably by virtue of membrane stabilizing properties. All drugs effective in migraine therapy oppose PG synthesis or antagonize its action. The understanding of prostaglandins physiology permits a more rational approach to migraine therapy than has been possible in the past.