02255nas a2200277 4500008004100000022001400041245007400055210006900129260001300198300001000211490000700221520148400228653001001712653002501722653001901747653004101766653001101807653001101818653002001829653001401849653000901863653001601872653001401888100001601902856005901918 1998 eng d a0011-905900aImmunoregulatory mechanisms and stress hormones in psoriasis (part 1)0 aImmunoregulatory mechanisms and stress hormones in psoriasis par c1998 May a350-70 v373 a

BACKGROUND: In an earlier paper, the author noted that psoriatic eruptions may be produced in phases of humoral and cellular immunodeficiency and in the presence of streptococcal antigen-releasing inflammatory foci. In this study it was investigated as to whether stress hormones glucocorticoids, catecholamines) are substantially involved in the activity phases (eruptions) of psoriasis.

METHODS: During a series of investigations over two years, the following were determined for 70 chronic psoriasis patients and 50 controls: cortisol-adrenaline serum levels, polyclonal serum immunoglobulins IgM, IgG, IgA, total serum IgE, complements C3, C4, T-cells and subpopulations, streptococcal antibody titres ASO/ADNase B.

RESULTS: Phases of clinical inactivity are associated with a mechanism called immunologic regulation: elevated antibacterial titres and unremarkable findings for all other parameters. Phases of clinical activity (in 25/70 patient) showed absolutely elevated serum cortisol levels, absolutely decreased serum epinephrine levels, deficient serum IgM or IgG and IgE levels, increased C3, decreased C4 and T4:T8 ratio, and significantly elevated streptococcal titres.

CONCLUSIONS: The greatly elevated serum cortisol levels indicate that glucocorticoids are produced in excess via the pituitary adrenal axis and are significantly involved in the triggering of immunosuppressive phases (eruptions) in psoriasis.

10aAdult10aCase-Control Studies10aCatecholamines10aChromatography, High Pressure Liquid10aFemale10aHumans10aImmunoglobulins10aInfection10aMale10aMiddle Aged10aPsoriasis1 aWeigl, B, A uhttp://www.microfluidicsciences.com/drupal/?q=node/230