Zusammenfassung
Bei der Psoriasis handelt es sich um eine polygenetisch vererbbare multifaktoriell
bedingte Erkrankung, die durch zahlreiche Umwelteinflüsse beeinflussbar ist. Es gibt
bisher kaum Studien, die den Einfluss von Stress auf die Psoriasis experimentell untersuchten.
Ein Problem der vorhandenen Studien ist, dass unklar bleibt, ob die experimentellen
Befunde für die Gesamtgruppe der Patienten relevant ist oder ob es Untergruppen gibt,
die besonders stressanfällig sind. Hauptziel dieser Studie ist es daher, zu untersuchen,
ob sich mit einem experimentellen Stressor Untergruppen von Patienten finden, die
besonders stressanfällig sind und dies auch durch Veränderungen immunologischer Parameter
sichtbar wird. Methode: Als Stressor wurde der TSST (Trierer-Social-Stress-Test) eingesetzt. Der Schweregrad wurde sowohl objektiv anhand des PASI (Psoriasis Area Severity Index) sowie subjektiv durch den Patienten erfasst. Als somatische Parameter, die innerhalb
dieser Studie explorativ untersucht wurden, wurden Parameter gewählt, von denen die
Stressreagibilität bekannt ist, aber kein direkter Bezug zur Psoriasis angenommen
werden kann (Speichelkortisol). Als zweite Gruppe von Parametern wurden Variablen
gewählt, bei denen ein Zusammenhang mit der Pathophysiologie der Psoriasis und/oder
dem Schweregrad bekannt war, bei denen die Stressreagibilität aber unklar war. Neben
Speichelkortisol wurden aus dem Serum Eosinophile, ICAM-3 und sIL-2R bestimmt. Es
wurden 38 Psoriatiker und 38 Kontrollpersonen untersucht. Es nahmen je 21 Männer und
17 Frauen an der Studie teil. Ergebnisse: Der PASI korrelierte dabei sehr unterschiedlich mit den subjektiven Schweregradparametern.
Die Zusammenhänge zwischen Schweregrad und den von uns untersuchten Blutparametern
ergab nur für die Eosinophilen eine systematische Beziehung. Der TSST ist geeignet,
auch bei Psoriatikern Stress auszulösen. Bei einer Untergruppe kommt es zu einem Anstieg
des Hautbefalls, während bei der zweiten Untergruppe der Hautbefall infolge des Experimentes
abnimmt oder konstant bleibt. Mit den untersuchten immunologischen Parametern lässt
sich die Klassifizierung in stressreagible und nonreagible Patienten allerdings nicht
stützen.
Abstract
Psoriasis is a polygenetic hereditary multifactorial disease which may be influenced
by a number of environmental factors. To date only a few studies experimentally investigated
the influence of stress on psoriasis. One problem of these studies is that it remains
unclear whether the experimental findings are relevant for the entire group of patients,
or whether there are subgroups who are particularly susceptible to stress. Therefore
our main objective is to examine whether experimental stressors can identify subgroups
of patients who are particularly susceptible to stress and if these differ in immunological
parameters. Method: The Trier Social Stress Test (TSST) was used as stressor. The severity was recorded
both objectively using the PASI (Psoriasis Area and Severity Index) as well as subjectively
by the patient. Somatic parameters for which stress reactivity is known but no direct
relationship to psoriasis is assumed were selected and exploratively examined within
the present study (salivary cortisol). The second set of parameters for which the
stress reactivity was unclear included variables which are linked to the pathophysiology
and/or the severity of psoriasis. In addition to salivary cortisol, eosinophils, ICAM-3,
and sIL-2R were determined in serum. 38 psoriasis patients and 38 control subjects
were examined (21 male and 17 female participants within each group). Results: The PASI correlated very inconsistently with the subjective severity parameters.
The relationships between severity and blood parameters tested showed a systematic
relationship for eosinophils only. The TSST is suitable for eliciting stress in psoriasis
patients. In one subgroup, there was an increase in skin affliction, while skin affliction
in the second group remained constant or decreased. A classification into stress-reactive
or non-reactive patients cannot, however, be supported by the immunological parameters
tested.
Key words
Skin - psoriasis - stress - pruritus - psycho-social
Literatur
- 1 Augustin M, Schöpf E. Psoriasis. Ursachen und Therapie der Schuppenflechte. München;
Beck 1999
- 2
Barker N WN.
Genetic aspects of psoriasis.
Clin Exp Dermatol.
2001;
26
321-325
- 3
Gupta M A, Gupta A K, Schork N J, Ellis C N.
Depression modulates pruritus perception: a study of pruritus in psoriasis, atopic
dermatitis and chronic idiopathic urticaria.
Psychosom Med.
1994;
56
36-40
- 4 Newbold P CH. Pruritus in psoriasis. In: Psoriasis, Proceedings of the Second International
Symposium. Stanford University 1976. New York; Yorke Medical Books 1977: 334
- 5
Yosipovitch G, Goon A, Wee J. et al .
The prevalence and clinical characteristics of pruritus among patients with extensive
psoriasis.
Br J Dermatol.
2000;
143
969-973
- 6
Griffiths C E, Richards H L.
Psychological influences in psoriasis.
Clin Exp Dermatol.
2001;
26
338-342
- 7
Picardi A, Abeni D.
Stressful life events and skin diseases: disentangling evidence from myth.
Psychother Psychosom.
2001;
70
118-136
- 8
Stangier U.
Feldstudien zur belastungsbedingten Reaktivität von Hauterkrankungen. Eine methodenkritische
Übersicht.
Verhaltensmod Verhaltensmed.
1995;
16
353-371
- 9
Al'Abadie M S, Kent G G, Gawkrodger D J.
The relationship between stress and the onset and exacerbation of psoriasis and other
skin conditions.
Br J Dermatol.
1994;
130
199-203
- 10
Gieler U, Niemeier V, Kupfer J. et al .
Psychosomatische Dermatologie in Deutschland. Eine Umfrage an 69 Hautkliniken.
Hautarzt.
2001;
52
104-110
- 11
Farber E M, Nall L.
The natural history of psoriasis in 5600 patients.
Dermatologica.
1974;
148
1-18
- 12
Gaston L, Lassonde M, Bernier-Buzzanga J. et al .
Psoriasis and stress: a prospective study.
J Am Acad Dermatol.
1987;
17
82-86
- 13
Seville R H.
Psoriasis and stress I.
Br J Dermatol.
1977;
97
297-302
- 14
Seville R H.
Psoriasis and stress II.
Br J Dermatol.
1978;
98
151-153
- 15
Suljagic E, Sinanovic O, Tupkovic E, Moro L.
Stressful life events and psoriasis during the war in Bosnia.
Dermatol Psychosom.
2000;
1
56-61
- 16
Gupta M A, Gupta A K, Kirkby S. et al .
A psychocutaneous profile of psoriasis patients who are stress reactors.
Gen Hosp Psych.
1989;
11
166-173
- 17
Scharloo M, Kaptein A A, Weinman J. et al .
Patients' illness perceptions and coping as predictors of functional status in Psoriasis:
a 1-year follow-up.
Br J Dermatol.
2000;
142
899-907
- 18
Scharloo M, Kaptein A A, Weinman J. et al .
Illness perceptions, coping and functioning in patients with rheumatoid arthritis,
chronic obstructive pulmonary disease and psoriasis.
J Psychosom Res.
1998;
44
573-585
- 19
Niemeier V, Nippesen M, Kupfer J. et al .
Hand eczema - Should psychological factors be considered in etiology or treatment?.
Br J Dermatol.
2002;
146
1031-1037
- 20
Stangier U, Gieler U, Ehlers A.
Measuring Adjustment to Chronic Skin Disorders: Validation of a Self-Report Measure.
Psychological Assessment.
2003;
15
532-549
- 21
Arnetz B B, Fjellner B, Eneroth P, Kallner A.
Stress and psoriasis: psychoendocrine and metabolic reactions in psoriatic patients
during standardized stressor exposure.
Psychosom Med.
1985;
47
528-541
- 22
Schmid-Ott G, Jacobs R, Jäger B. et al .
Stress-induced endocrine and immunological changes in psoriasis patients and healthy
controls. A preliminary study.
Psychother Psychosom.
1998;
67
37-42
- 23
Schmid-Ott G, Jaeger B, Adamek C. et al .
Circulating CD8+T lymphocytes, NK cells and eosinophils increase upon acute psychosocial
stress in patients with atopic dermatitis.
J Allergy Clin Immunol.
2001;
107
171-177
- 24
Weigl B A.
Immunregulatory mechanisms and stress hormones in psoriasis (part 1).
Int J Dermatol.
1998;
37
350-357
- 25
Thaller V, Vrkljan M, Hotujac L, Thakore J.
The potential role of hypocortisolism in the pathophysiology of PTSD and psoriasis.
Coll Antropol.
1999;
23
611-619
- 26
Kirschbaum C, Pirke K M, Hellhammer D H.
The Trier Social Stress Test - a tool for investigating psychobiological stress responses
in a laboratory setting.
Neuropsychobiology.
1993;
28
76-81
- 27
Fredriksson T, Pettersson U.
Severe psoriasis - oral therapy with a new retinoid.
Dermatologica.
1978;
157
238-244
- 28
Feldman S R, Fleischer A B, Reboussin D M. et al .
The self-administered psoriasis area and severity index is valid and reliable.
J Invest Dermatol.
1996;
106
183-186
- 29
Biondi M, Picardi A.
Psychological stress and neuroendocrinic function in humans: The last two decades
of research.
Psychother Psychosom.
1999;
68
114-150
- 30
Lundin A, Fredens K, Michaelsson G, Venge P.
The eosinophil granulocyte in psoriasis.
Br J Dermatol.
1990;
122
181-193
- 31
Shupack J L, Kenny C, Jondreau L. et al .
Decreased peripheral blood eosinophil counts in severe psoriatic patients treated
with low-dose cyclosporine A.
Dermatology.
1992;
185
202-204
- 32
Venge P.
The human eosinophil in inflammation.
Agents Actions.
1990;
29
122-126
- 33
Glaser R, Kennedy S, Lafuse W P. et al .
Psychological stress-induced modulation of interleukin-2 receptor gene expression
and interleukin-2 production in peripheral blood leukocytes.
Arch Gen Psychiat.
1990;
47
707-712
- 34
Maes M, Bosmans E, Suy E. et al .
Depression-related disturbances in mitogen-induced lymphocyte responses and interleukin-1
and soluble interleukin-2 receptor production.
Acta Psychiat Scand.
1991;
84
379-386
- 35
Bos J D, Rie M A De.
The pathogenesis of psoriasis: immunological facts and speculations.
Immunol Today.
1999;
20
40-46
- 36
Rie M A De, Out T A, Bos J D.
Low-dose narrow-band UVB phototherapy combined with topical therapy is effective in
psoriasis and does not inhibit systemic T-cell activation.
Dermatology.
1998;
196
412-417
- 37
Kapp A, Neuner P, Krutmann J. et al .
Production of interleukin-2 by mononuclear cells in vitro in patients with atopic
dermatitis and psoriasis. Comparison with serum interleukin-2 receptor levels.
Acta Derm Venereol.
1991;
71
403-406
- 38
Pita O De, Ruffelli M, Cadoni S. et al .
Psoriasis: comparison of immunological markers in patients with acute and remission
phase.
J Dermatol Sci.
1996;
13
118-124
- 39
Rie M A De, Hamerlinck F, Hintzen R Q. et al .
Quantitation of soluble CD27, a T-cell activation antigen, and soluble interleukin-2
receptor in serum from patients with psoriasis.
Arch Dermatol Res.
1991;
283
533-534
- 40
Gebhardt M, Wenzel H C, Hipler U C. et al .
Monitoring of serologic immune parameters in inflammatory skin diseases.
Allergy.
1997;
52
1087-1094
- 41
Rie M A De, Zonneveld I M, Witkamp L. et al .
Soluble interleukin-2 receptor (sIL-2R) is a marker of disease activity in psoriasis:
A comparison of sIL-2R, sCD27, sCD4, sCD8 and sICAM-1.
Acta Derm Venereol.
1996;
76
357-360
- 42
Elkayam O, Yaron I, Shirazi I. et al .
Serum levels of IL-10, IL-6, IL-1ra, and sIL-2R in patients with psoriatic arthritis.
Rheumatol Int.
2000;
19
101-105
- 43
Griffith C E, Railan D, Gallatin W M, Cooper K D.
The ICAM-3/LFA-1 interaction is critical for epidermal Langerhans cell alloantigen
presentation to CD4+ T cells.
Br J Dermatol.
1995;
133
823-829
- 44
Griffith C E, Boffa M J, Gallatin W M, Martin S.
Elevated levels of circulating intercellular adhesion molecule-3 (cICAM-3) in psoriasis.
Acta Derm Venereol.
1996;
76
2-5
- 45
Bell L M, Sedlack R, Beard M C. et al .
Incidence of psoriasis in Rochester, Minn 1980 - 1983.
Arch Dermatol.
1991;
127
1184-1187
- 46
Kirby B, Fortune D G, Bhushan M. et al .
The Salford Psoriasis Index: an holistic measure of psoriasis severity.
Br J Dermatol.
2000;
142
728-732
- 47 Kupfer J. Die Stressabhängigkeit von Neurodermitis, Psoriasis und Urticaria. Habilitationsschrift
am Fachbereich Humanmedizin. Gießen; Justus-Liebig-Universität 2001
- 48
Buske-Kirschbaum A, Jobst S, Wustmans A. et al .
Attenuated free cortisol response to psychosocial stress in children with atopic dermatitis.
Psychosom Med.
1997;
59
419-426
- 49
Buske-Kirschbaum A, Geiben A, Hellhammer D.
Psychobiological aspects of atopic dermatitis: an overview.
Psychother Psychosom.
2001;
70
6-16
Priv.-Doz. Dr. Jörg Kupfer
Abteilung für Medizinische Psychologie
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eMail: joerg.p.kupfer@psycho.med.uni-giessen.de