B A Weigl1. 1. Private Dermatology Practice 1040, Vienna, Austria.
Abstract
BACKGROUND: In an earlier paper, it was described how acute eruptions of psoriasis may be produced in phases of immune deficiency and in the presence of bacterial antigen-releasing inflammatory foci, whereas clinical spontaneous remissions are produced in phases of immunologic activity. Therefore, it was of interest to investigate whether the stress hormones cortisol/epinephrine are involved in triggering such deficiency and activity phases. METHODS: During a series of investigations lasting up to 3 years in 95 patients, the following were determined: cortisol/epinephrine levels, polyclonal serum immunoglobulins IgM, IgG, and IgA, total serum IgE, complement C3 and C4 proteins, T cells and subpopulations, as well as streptococcal titers ASO/ADNase B, severity index (PASI) RESULTS: Phases of clinical inactivity are associated with the mechanism, "immunologic regulation," where antibacterial titers are elevated, but all other parameters are unremarkable. Eruption phases (in 32 of 95 patients) showed absolute increases in serum cortisol levels and antibacterial titers, and decreases in serum epinephrine (adrenaline) levels. Phases of spontaneous remission (in 25 of 32 patients) showed, in contrast to the eruption phases, absolute increases in serum epinephrine levels, and significant falls in serum cortisol levels and bacterial titers. CONCLUSIONS: On the basis of these results, the participation of the immune system is confirmed in the pathogenesis of psoriasis, which is subject to control by higher neurohormonal systems. Cortisol may be involved in the clinical eruption phase, and epinephrine in the remission phase. Both hormones are true antagonists and have important effects on the human immune system if produced in excess via the pituitary-adrenal axis. Infection with Streptococcus pyogenes is an additional trigger for the dermatosis.
BACKGROUND: In an earlier paper, it was described how acute eruptions of psoriasis may be produced in phases of immune deficiency and in the presence of bacterial antigen-releasing inflammatory foci, whereas clinical spontaneous remissions are produced in phases of immunologic activity. Therefore, it was of interest to investigate whether the stress hormones cortisol/epinephrine are involved in triggering such deficiency and activity phases. METHODS: During a series of investigations lasting up to 3 years in 95 patients, the following were determined: cortisol/epinephrine levels, polyclonal serum immunoglobulins IgM, IgG, and IgA, total serum IgE, complement C3 and C4 proteins, T cells and subpopulations, as well as streptococcal titers ASO/ADNase B, severity index (PASI) RESULTS: Phases of clinical inactivity are associated with the mechanism, "immunologic regulation," where antibacterial titers are elevated, but all other parameters are unremarkable. Eruption phases (in 32 of 95 patients) showed absolute increases in serum cortisol levels and antibacterial titers, and decreases in serum epinephrine (adrenaline) levels. Phases of spontaneous remission (in 25 of 32 patients) showed, in contrast to the eruption phases, absolute increases in serum epinephrine levels, and significant falls in serum cortisol levels and bacterial titers. CONCLUSIONS: On the basis of these results, the participation of the immune system is confirmed in the pathogenesis of psoriasis, which is subject to control by higher neurohormonal systems. Cortisol may be involved in the clinical eruption phase, and epinephrine in the remission phase. Both hormones are true antagonists and have important effects on the human immune system if produced in excess via the pituitary-adrenal axis. Infection with Streptococcus pyogenes is an additional trigger for the dermatosis.