Psychosomatic Medicine
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Modell, J. G.
Right arrow Articles by Katholi, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Modell, J. G.
Right arrow Articles by Katholi, C.
Related Collections
Right arrow Consultation Psychiatry
Right arrow Dermatology
Psychosomatic Medicine 64:835-840 (2002)
© 2002 American Psychosomatic Society

ORIGINAL ARTICLES

Treatment of Atopic Dermatitis and Psoriasis Vulgaris With Bupropion-SR: A Pilot Study

Jack G. Modell, MD, Sarah Boyce, MD, Eric Taylor, MD and Charles Katholi, PhD

From the Departments of Psychiatry (J.G.M., E.T.), Dermatology (S.B.), and Biostatistics (C.K.), the University of Alabama at Birmingham School of Medicine, Birmingham, AL.

Address reprint requests to: Jack G. Modell, Professor of Psychiatry, University of Alabama at Birmingham School of Medicine, 1700 7th Avenue South, Room 219, Birmingham, AL 35294-0018. Email: jgmodell{at}earthlink.net


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
OBJECTIVE: To determine whether the antidepressant bupropion may be useful in treating atopic dermatitis and psoriasis in nondepressed patients.

METHOD: Ten nondepressed subjects with atopic dermatitis and 10 with psoriasis completed a single-track, open-label treatment protocol with bupropion-SR in doses of 150 mg/day and 300 mg/day, administered sequentially for 3 weeks each, followed by a 3-week wash-out. Treatment response was assessed at the end of each 3-week period.

RESULTS: Six of the 10 subjects with atopic dermatitis showed a reduction in affected body surface area by the end of 6 weeks of bupropion treatment, with affected area increasing toward the prestudy baseline in all responders following bupropion discontinuation—a highly significant treatment effect (p = .0003). Of the 10 subjects having psoriasis, improvement over baseline after 6 weeks of treatment was seen in eight subjects, with coverage increasing toward the prestudy baseline in the responders following bupropion discontinuation (p = .001). Average reduction in affected area in the responders at week 6 of treatment was approximately 50% in both groups.

CONCLUSIONS: The generally good tolerability and relative safety of bupropion-SR makes a trial of this agent worthwhile in patients with atopic dermatitis or psoriasis who have failed treatment with more conventional medications. Normalization by bupropion of potentially causative neuroendocrine, immunologic, or catecholaminergic abnormalities in both of these dermatologic disorders is a possible mechanism of action for the observed salutary effects of this drug on our subjects’ skin disease.

Key Words: antidepressant, • atopic dermatitis, • bupropion, • eczema, • psoriasis.

Abbreviations: ANCOVA = analysis of covariance;; bupropion-SR = bupropion sustained-release formulation (GlaxoSmithKline Pharmaceuticals);; DSM-IV = Diagnostic and Statistical Manual of Mental Disorders, 4th edition;; hCRH = human corticotrophin-releasing hormone;; HPA = hypothalamic-pituitary-adrenal.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
In a recent study assessing the efficacy of the aminoketone antidepressant bupropion-SR (1) (Wellbutrin-SR, GlaxoSmithKline) as a treatment for orgasmic dysfunction in nondepressed individuals (2), one of our subjects who had suffered from treatment-refractory atopic dermatitis (eczema) for about 15 years noted an unexpected and unprecedented clearing of all skin disease after about 5 weeks on 150–300 mg/day of the bupropion and a subsequent return of the dermatitis to its previous severity about 3 weeks after bupropion was discontinued. Although a call to the drug’s manufacturer regarding these findings revealed that they had received a few sporadic reports of patients with atopic dermatitis and also psoriasis vulgaris (henceforth, psoriasis) whose skin had cleared during treatment with bupropion, no reports of the effect of bupropion on dermatologic disorders could be found in the medical literature. There have, however, been published reports of improvement of atopic dermatitis with topical application of the strongly antihistiminergic tricyclic antidepressant doxepin (3, 4) and of psoriasis with oral administration the tricyclic antidepressant imipramine (5, 6) and with the monoamine-oxidase inhibitor moclobemide (7).

In an effort to determine whether orally administered bupropion might indeed have beneficial effects on skin disease in nondepressed patients with atopic dermatitis and psoriasis, we conducted the following pilot study.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Adult subjects with atopic dermatitis or psoriasis diagnosed by a dermatologist were eligible to participate in this study if their skin disease had been present continuously for at least 1 year, had not changed in intensity or coverage during the 3 months preceding the study, and had not previously cleared with topical treatment. Excluded from participation were subjects using oral or topical dermatologic medications within the preceding month; subjects having any signs or symptoms of depression, anxiety disorder, mania, psychosis, or history thereof (DSM-IV criteria (8)); subjects having any major medical illness, epilepsy, or eating disorder; and subjects taking any antidepressant medication. Specifically with regard to depression, no subject reported depressed mood and no subject had more than one of the nine required DSM-IV criteria for depression (8). The study was approved by the university’s investigational review board, and informed consent was obtained from all study subjects.

Thirteen subjects having atopic dermatitis and 11 with psoriasis were inducted into the study. Of the three subjects with atopic dermatitis who did not complete the study, one failed to return after the initial visit, citing inconvenience as the reason, and two failed to return after the second visit despite both reporting that the bupropion was helpful (one cited inconvenience and the other moved from the area). Of the subjects with psoriasis, 10 completed the study: the one noncompleter failed to return after the first visit and did not return our follow-up calls. Subject characteristics of the 20 completers included in the data analysis are shown in Table 1 (atopic dermatitis) and Table 2 (psoriasis). The median duration of continuous disease presence before participation in subjects with atopic dermatitis was 10 years (range 1–15 years) and, in subjects with psoriasis, 20 years (range 3–45 years).


View this table:
[in this window]
[in a new window]
  		Table 1. Demographic and Clinical Characteristics of Subjects Having Atopic Dermatitisa
 

View this table:
[in this window]
[in a new window]
  		Table 2. Demographic and Clinical Characteristics of Subjects Having Psoriasisa
 
The study was designed as a single-track, open-label protocol of two sequential doses of bupropion-SR followed by medication discontinuation over a period of 9 weeks. At the time of the initial evaluation, medical, psychiatric, and dermatologic histories were obtained and the skin was examined with attention to disease appearance and percent coverage of the affected body area(s) as measured to the closest 25% (Table 1 and Table 2). Also recorded was whether the subjects believed their skin disease worsened under psychological stress.

Subjects were then placed on bupropion-SR 150 mg by mouth each morning for 3 weeks, at which time the subjects returned to the clinic for evaluation of drug effect. Bupropion-SR dosage was then increased to 150 mg by mouth twice daily until the second follow-up visit 3 weeks later; subjects who felt that 150 mg/d was adequate or were having any bothersome side effects, however, had the option of remaining on 150 mg daily for the second dosing period. At the time of the second follow-up visit (week 6 of the study), the skin was reexamined and the bupropion was discontinued. The final clinical evaluation occurred 3 weeks following bupropion discontinuation (week 9). Qualitative changes in skin condition by examination and patient report were recorded for each subject, and changes in measured affected surface area were rated relative to that observed at the initial evaluation as closest to a >=75% reduction (-3), 50% reduction (-2), 25% reduction (-1), no change (0), 25% increase (+1), 50% increase (+2), or >=75% increase (+3). Additionally, subjects were asked at each follow-up visit whether any psychiatric symptoms, particularly those of depression, had emerged.

Outcome data regarding changes in skin condition as well as potential covariate effects (age, sex, race, extent of disease coverage, whether or not the subjects considered their dermatitis to be stress related, duration of the dermatitis before study participation, and bupropion dose) were analyzed using a one-way, repeated-measures ANCOVA model for treatment effect (SAS procedure MIXED). An autocorrelation (AR (1)) structure was incorporated into the analysis to adjust for possible nonindependence of the within-subjects observations in this longitudinal data (9). Tests of treatment effect were one sided; covariate analyses were two sided.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Quantitative changes in affected surface area relative to the prestudy baseline are shown in Table 3 (atopic dermatitis) and Table 4 (psoriasis). Of the 10 subjects having atopic dermatitis, observable decreases relative to baseline in affected surface area after 3 weeks on bupropion-SR 150 mg/day were rated as closest to 25% in three, and one subject’s skin disease cleared entirely (subject A4); no effect was observed in six subjects (t27 = 1.8, p = .04 for week 3 vs. baseline). Three weeks later, with eight subjects taking 300 mg/day bupropion-SR and two remaining on 150 mg/day, 6 of the 10 subjects showed decreases in affected surface area over baseline, three of which were rated as 50% and three as >=75%; four subjects’ disease remained unchanged, and the one subject whose disease cleared entirely at week 3 had a return of one small patch of dermatitis by week 6 (t27 = 4.6, p < .0001 for week 6 vs. baseline; t27 = 2.8, p = .005 for week 6 vs. week 3). Average reduction in affected surface area at week 6 in the responders was approximately 50%. In all cases, decreases in affected surface area were associated with subjective reports of improvement in disease coverage, intensity, irritation, and pruritus.


View this table:
[in this window]
[in a new window]
  		Table 3. Change Scores for Disease Coverage Relative to Baseline at Each Evaluation Period for Patients With Atopic Dermatitis; >=75% Reduction (-3), 50% Reduction (-2), 25% Reduction (-1), No Change (0), 25% Increase (+1), 50% Increase (+), or >=75% Increase (+3)
 

View this table:
[in this window]
[in a new window]
  		Table 4. Change Scores for Disease Coverage Relative to Baseline at Each Evaluation Period for Patients With Psoriasisa
 
Three weeks following discontinuation of the bupropion-SR, each of the subjects whose atopic dermatitis improved on the medication showed an increase in affected surface area over that present at week 6, with skin disease in three of these subjects returning to its prestudy condition (t27 = -3.7, p = .0005 for week 9 vs. week 6; t27 = -0.92, p = .37 for week 9 vs. baseline). Skin disease in three subjects remained unchanged throughout the 9-week protocol, and one subject’s disease remained unchanged during bupropion administration yet increased in affected area by approximately 25% following its discontinuation. An overall treatment effect was highly significant (F3,27 = 7.9, p = .0003). There were no significant correlations between treatment effect and age, sex, race, extent of disease coverage, whether or not the subjects considered their skin disease to be stress related, duration of the skin disease before study participation, or bupropion dose.

Three of the six subjects who appeared to have a positive response to bupropion expressed a desire to resume the medication for long-term treatment of their atopic dermatitis; those who did not expressed dislike of "dependence on [systemic] medication." One of these responders (A1) was subsequently treated with bupropion 300 mg/day by the first author and remained disease free at a 3-month follow-up.

Of the 10 subjects having psoriasis, observable decreases in affected surface area relative to baseline after 3 weeks on bupropion-SR 150 mg/day were rated as closest to 25% in one, 50% in one, and >=75% in one; one subject’s disease increased in surface area by 25%, six were unchanged, and no subject’s skin disease cleared entirely (t27 = 1.24, p = .11 for week 3 vs. baseline). Three weeks later, with nine subjects taking 300 mg/day bupropion-SR and one remaining on 150 mg/day, 8 of the 10 subjects showed decreases in affected surface area over baseline, three of which were rated as 25%, two as 50%, and three as >=75%; skin disease in two subjects remained unchanged (t27 = 4.0, p = .0002 for week 6 vs. baseline; t27 = 2.7, p = .005 for week 6 vs. week 3). Average reduction in disease coverage at week 6 in the responders was approximately 50%. In all cases, decreases in affected surface area were associated with subjective reports of improvement in disease coverage, intensity, irritation, and pruritus.

Three weeks following discontinuation of the bupropion-SR, each of the subjects whose psoriasis improved on bupropion-SR showed an increase in affected surface area over that present at week 6, with skin disease increasing to its baseline condition in four of these subjects and exceeding baseline coverage by about 25% in one (t27 = -3.5, p = .001 for week 9 vs. week 6; t27 = 0.50, p = .62 for week 9 vs. baseline). Skin disease in two subjects remained unchanged and no subject’s disease cleared completely during the study period. An overall treatment effect was highly significant (F3,27 = 6.3, p = .001). As with subjects having atopic dermatitis, there were no significant correlations between treatment effect and any of the covariates.

Six of the eight subjects whose psoriasis responded positively to bupropion-SR expressed a desire to resume the medication for long-term treatment of their psoriasis; again, those who did not cited dislike of long-term oral medication use. Of the two of these six subjects who were personally treated by the first author, the initial benefit waned after about 3 months in one (P2), but in the other (P1), there was complete clearing of all skin disease 1 month after resuming the medication and—save for one small plaque—the psoriatic lesions have yet to return after 19 months.

The bupropion-SR was generally well tolerated, and no subjects dropped out due to side effects. Specific side effects that occurred in more than 1 of the 20 subjects were limited to dizziness (N = 2), restless sleep or increased dreaming (N = 2), subjective tachycardia (N = 3), and feeling "jittery" or "wired" (N = 3). Only one subject (P8) felt that the bupropion improved his mood beyond his nondepressed baseline; no other subject reported any change in mood or the emergence of depressive symptoms.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
That a highly significant treatment effect was found, with skin disease in 6 out of 10 subjects with atopic dermatitis and 8 out of 10 with psoriasis improving by week 6 of this study and all of the responders in both groups worsening within 3 weeks of discontinuing bupropion, suggests that orally administered bupropion may be useful in treating both of these disorders. Also arguing for a significant drug effect is that the observed improvements occurred in patients with very chronic, relatively static skin disease that had not previously responded well to topical treatment and also that one subject with particularly severe psoriasis for 18 years remains nearly disease free 19 months into bupropion treatment. The absence of a control group and blinding in this study does not, however, allow exclusion of a significant placebo response. That no significant correlations were found between treatment effect and age, sex, race, extent of disease coverage, whether or not the subjects considered their dermatitis to be stress related, duration of the dermatitis before study participation, and bupropion dose is noteworthy, but the number of subjects is too small to conclude that these factors are indeed inconsequential.

A mechanism of action for the observed improvements is difficult to postulate because bupropion has no known effect on skin, its only known action being a weak inhibitor of norepinephrine and dopamine uptake in the brain (1, 10, 11). Although many studies have shown a higher rate of anxiety, depression, intrapsychic conflict, and perceived stress levels in patients with both atopic dermatitis and psoriasis (12–20), the absence of an association in this study between improvement and whether subjects perceived their dermatitis to be stress related as well as the absence of a general effect of bupropion on subject mood would argue against improvement being related to a specific antidepressant or psychological effect of bupropion.

More plausible, however, are potential neuroendocrine, immunologic, or catecholaminergic mechanisms of action for bupropion on these skin disorders. Several studies have shown that a number of antidepressants have neuroendocrine and immunologic effects, including decreasing natural-killer cell activity and inflammatory response in mice; decreasing macrophage migration and hypersensitivity reactions in rats (21–24); and in humans, altering concentrations of opioid peptides and beta-endorphin concentrations in lymphocytes (25), suppressing natural-killer cell activity (26), altering interferon/interleukin production ratios (27), normalizing the chronic hypothalamic-pituitary-adrenocortical (HPA) axis overactivity in patients with depression (21, 28–30), and inhibiting the substance-P inflammatory response in skin (31). Such findings, however, have not yet been specifically demonstrated with bupropion. Additionally, the antidepressants, including bupropion, have been shown to enhance central noradrenergic transmission by decreasing the sensitivity of postsynaptic alpha-2 adrenergic receptors (32) and decreasing the firing rates of noradrenergic neurons in the locus ceruleus (1) while reducing whole-body turnover of norepinephrine (33) and plasma levels of norepinephrine and its metabolites 3-methoxy-4-hydroxyphenylglycol and dihydroxyphenylglycol (1, 32, 34–36).

Interestingly, neuroendocrine, immunologic, and catecholaminergic abnormalities have all been implicated in the pathogenesis of both atopic dermatitis and psoriasis. Patients with atopic dermatitis show an attenuated response of the hypothalamic-pituitary-adrenal system during a human corticotrophin-releasing hormone (hCRH) challenge (37), increased IgE-production and mediator secretion and T-lymphocyte regulatory disturbances (38, 39), and decreased natural-killer cell function (40). Catecholaminergic abnormalities in atopic dermatitis include impaired beta-adrenergic and enhanced alpha-adrenergic reactivity (41, 42), elevated plasma levels of norepinephrine (43, 44), and an abnormally low density of beta-2-adrenergic surface receptors on skin keratinocytes (45). As these receptors respond to circulating catecholamines by regulating calcium influx and thereby controlling cell differentiation (45), such systemic or cellular abnormalities could give rise to the abnormal epidermal development observed in atopic dermatitis. It is also not inconceivable that, because both the skin and brain are derived from embryologic cell populations adjacent to the neural crest (46), there is enough commonalty between these tissues that bupropion may have specific effects of its own on adrenergic receptors in dermal or epidermal tissue. Hypocortisolism and abnormalities in the function of the HPA axis (47), abnormalities in T-lymphocyte reactivity and release of associated inflammatory cytokines in the skin (48–51), and relatively high concentrations of circulating norepinephrine (52) have also been observed in patients with psoriasis. Additionally, there is increasing evidence that abnormalities in neurotensin and substance-P receptors or production in the skin may be involved in the pathogenesis of both atopic dermatitis and psoriasis (53, 54).

Normalization by bupropion of any of these potentially causative abnormalities in atopic dermatitis and psoriasis is thus theoretically possible and may explain the observed salutary effects of this drug on our subjects’ skin disease. At this time, however, each of these mechanistic possibilities must be considered speculative and it is not possible to narrow them much further; if, however, it can be shown that noncatecholaminergic antidepressants (such as the selective-serotonin reuptake inhibitor antidepressants) also have a beneficial effect in these disorders, then a catecholaminergic mechanism of action for bupropion in these dermatologic disorders would be considerably less likely.

Further research will be necessary to confirm our findings and to clarify possible mechanisms of action for the observed dermatologic effects of bupropion-SR in this study. Until such time that these can be completed, however, we believe that the generally good tolerability and relative safety of bupropion-SR makes a trial of this agent worthwhile in patients with atopic dermatitis or psoriasis who have failed treatment with more conventional medications.

Received for publication June 20, 2001.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Ascher JA, Cole JO, Colin JN, Feighner JP, Ferris RM, Fibiger HC, Golden RN, Martin P, Potter WZ, Richelson E, Sulser F. Bupropion: a review of its mechanism of antidepressant activity. J Clin Psychiatry 1995; 56: 395–401.[Medline]
  2. Modell JG, May RS, Katholi CR. Effect of bupropion-SR on orgasmic dysfunction in non-depressed subjects. J Sex Marital Ther 2000; 26: 231–40.[CrossRef][Medline]
  3. Drake LA, Fallon JD, Sober A. Relief of pruritus in patients with atopic dermatitis after treatment with topical doxepin cream. J Am Acad Dermatol 1994; 31: 613–6.[Medline]
  4. Berberian BJ, Breneman DL, Drake LA, Gratton D, Raimir SS, Phillips S, Sulica VI, Bernstein JE. The addition of topical doxepin to corticosteroid therapy: an improved treatment regimen for atopic dermatitis. Int J Dermatol 1991; 38: 145–8.[CrossRef]
  5. Hardman R, Hopkins EJ, Pye AM, Solomon M, Solomon S. A trial of imipramine in the treatment of psoriasis. J Coll Gen Pract 1965; 10: 315–6.[Medline]
  6. Hebel E. Psoriasisbehandling med imipramin. Ugeskr Laeger 1966; 128: 20–1.
  7. Alpsoy E, Ozcan E, Cetin L, Ozgur O, Er H, Yilmaz E, Karaman T. Is the efficacy of topical corticosteroid therapy for psoriasis vulgaris enhanced by concurrent moclobemide therapy? J Am Acad Dermatol 1998; 38: 197–200.[CrossRef][Medline]
  8. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: The Association; 1994.
  9. Diggle P, Liang K-Y, Zeger S, Analysis of longitudinal data. Oxford, UK: Oxford University Press; 1994.
  10. Cooper BR, Wang CM, Cox RF, Norton R, Shea V, Ferris RM. Evidence that the acute behavioral and electrophysiological effects of bupropion (Wellbutrin) are mediated by a noradrenergic mechanism. Neuropsychopharmacology 1994; 11: 133–41.[Medline]
  11. Bassout A, Brinink A, Krauss J, Waldmeier P, Bischoff S. Regulation of dopamine receptors by bupropion: comparison with antidepressants and CNS stimulants. J Recept Res 1993; 13: 341–54.[Medline]
  12. Gupta MA, Gupta AK, Ellis CN, Voorhees JJ. Some psychosomatic aspects of psoriasis. Adv Dermatol 1990; 5: 21–31.[Medline]
  13. Gupta MA, Gupta AK, Kirkby S, Weiner HK, Mace TM, Schork NJ, Johnson EH, Ellis CN, Voorhees JJ. Pruritus in psoriasis. A prospective study of some psychiatric and dermatologic correlates. Arch Dermatol 1988; 124: 1052–7.[Abstract/Free Full Text]
  14. Ahmar H, Kurban AK. Psychological profile of patients with atopic dermatitis. Br J Dermatol 1976; 95: 373–7.[CrossRef][Medline]
  15. Fava GA, Perini GI, Santonastaso P, Fornasa CV. Life events and psychological distress in dermatologic disorders: psoriasis, chronic urticaria and fungal infections. Br J Med Psychol 1980; 53: 277–82.[Medline]
  16. Ginsburg IH, Prystowsky JH, Kornfeld DS, Wolland H. Role of emotional factors in adults with atopic dermatitis. Int J Dermatol 1993; 32: 656–60.[Medline]
  17. Hashiro M, Okumura M. Anxiety, depression and psychosomatic symptoms in patients with atopic dermatitis: comparison with normal controls and among groups of different degrees of severity. J Dermatol Sci 1997; 14: 63–7.[CrossRef][Medline]
  18. Brown DG. Stress as a precipitant factor of eczema. J Psychosom Res 1972; 16: 321–7.[CrossRef][Medline]
  19. Gupta MA, Gupta AK, Schork NJ, Ellis CN. Depression modulates pruritus perception: a study of pruritus in psoriasis, atopic dermatitis, and chronic idiopathic urticaria. Psychosom Med 1994; 56: 36–40.[Abstract/Free Full Text]
  20. Cotterill JA. Psychophysiological aspects of eczema. Semin Dermatol 1990; 9: 216–9.[Medline]
  21. Neveu PJ, Castanon N. Is there evidence for an effect of antidepressant drugs on immune function? Adv Exp Med Biol 1999; 461: 267–81.[Medline]
  22. Eisen JN, Irwin J, Quay J, Livnat S. The effect of antidepressants on immune function in mice. Biol Psychiatry 1989; 26: 805–17.[CrossRef][Medline]
  23. Audus KL, Gordon MA. Tricyclic antidepressant effects on the murine lymphocyte mitogen response. J Immunopharmacol 1982; 4: 13–27.[Medline]
  24. Basso AM, Depiante-Depaoli M, Cancela L, Molina V. Seven-day variable-stress regime alters cortical beta-adrenoceptor binding and immunologic responses: reversal by imipramine. Pharmacol Biochem Behav 1993; 45: 665–72.[CrossRef][Medline]
  25. Sacerdote P, Ciciliato IA, Rubboli F, Panerai AE. Effect of psychoactive drugs on lymphocyte neuropeptides. Ann N Y Acad Sci 1990; 594: 270–9.[Medline]
  26. Ravindran AV, Griffiths J, Merali Z, Anisman H. Lymphocyte subsets associated with major depression and dysthymia: modification by antidepressant treatment. Psychosom Med 1995; 57: 555–63.[Abstract/Free Full Text]
  27. Kubera M, Lin AH, Kenis G, Bosmans E, van Bockstaele D, Maes M. Anti-inflammatory effects of antidepressants through suppression of the interferon-gamma/interleukin-10 production ratio. J Clin Psychopharmacol 2001; 21: 199–206.[CrossRef][Medline]
  28. Stokes PE. The potential role of excessive cortisol induced by HPA hyperfunction in the pathogenesis of depression. Eur Neuropsychopharmacol 1995; 5 Suppl 1: 77–82.
  29. Akil H, Haskett RF, Young EA, Grunhaus L, Kotun J, Weinberg V, Greden J, Watson SJ. Multiple HPA profiles in endogenous depression: effect of age and sex on cortisol and beta-endorphin. Biol Psychiatry 1993; 33: 73–85.[CrossRef][Medline]
  30. Mokrani MC, Duval F, Crocq MA, Bailey P, Macher JP. HPA axis dysfunction in depression: correlation with monoamine system abnormalities. Psychoneuroendocrinology 1997; 22 Suppl 1: 63–8.
  31. Sabroe RA, Kennedy CT, Archer CB. The effects of topical doxepin on responses to histamine, substance P and prostaglandin E2 in human skin. Br J Dermatol 1997; 137: 386–90.[CrossRef][Medline]
  32. Charney DS, Heninger GR, Sternberg DE. Alpha-2 adrenergic receptor sensitivity and the mechanism of action of antidepressant therapy. The effect of long-term amitriptyline treatment. Br J Psychiatry 1983; 142: 265–75.[Abstract/Free Full Text]
  33. Golden RN, Rudorfer MV, Sherer MA, Linnoila M, Potter WZ. Bupropion in depression. I. Biochemical effects and clinical response. Arch Gen Psychiatry 1988; 45: 139–43.[Abstract/Free Full Text]
  34. Robinson DS, Johnson GA, Nies A, Corcella J, Cooper TB, Albright D, Howard D. Plasma levels of catecholamines and dihydroxyphenylglycol during antidepressant drug treatment. J Clin Psychopharmacol 1983; 3: 282–7.[Medline]
  35. Schildkraut JJ, Schatzberg AF, Samson JA, Rosenbaum A, Bowden CL. Norepinephrine output and metabolism in depressed patients during antidepressant treatments. Clin Neuropharmacol 1992; 15 Suppl 1, Pt A: 323–4.
  36. Frazer A. Norepinephrine involvement in antidepressant action. J Clin Psychiatry 2000; 61 Suppl 10: 25–30.
  37. Rupprecht M, Salzer B, Raum B, Hornstein OP, Koch HU, Riederer P, Sofic E, Rupprecht R. Physical stress-induced secretion of adrenal and pituitary hormones in patients with atopic eczema compared with normal controls. Exp Clin Endocrinol Diabetes 1997; 105: 39–45.[Medline]
  38. Thestrup-Pedersen K, Ellingsen AR, Olesen AB, Lund M, Kaltoft K. Atopic dermatitis may be a genetically determined dysmaturation of ectodermal tissue, resulting in disturbed T-lymphocyte maturation. A hypothesis. Acta Derm Venereol 1997; 77: 20–1.[Medline]
  39. Ring J, Dorsch W. Altered releasability of vasoactive mediator secreting cells in atopic eczema. Acta Derma Venereol Suppl 1985; 114: 9–23.
  40. Hashiro M, Okumura M. The relationship between the psychological and immunological state in patients with atopic dermatitis. J Dermatol Sci 1998; 16: 231–5.[CrossRef][Medline]
  41. Archer CB, Hanson JM, Morley J, MacDonald DM. Adrenoceptor function in atopic dermatitis: in vitro and in vivo observations. Acta Derm Venereol Suppl 1985; 114: 93–7.[Medline]
  42. Reed CE, Busse WW, Lee TP. Adrenergic mechanisms and the adenyl cyclase system in atopic dermatitis. J Invest Dermatol 1976; 67: 333–8.[CrossRef][Medline]
  43. Schallreuter KU, Pittelkow MR, Swanson NN, Beazley WD, Korner C, Ehrke C, Buttner G. Altered catecholamine synthesis and degradation in the epidermis of patients with atopic eczema. Arch Dermatol Res 1997; 289: 663–6.[CrossRef][Medline]
  44. Ionescu G, Kiehl R. Increased plasma norepinephrine in psoriasis. Acta Derm Venereol 1991; 71: 169–70.[Medline]
  45. Schallreuter KU. Epidermal adrenergic signal transduction as part of the neuronal network in the human epidermis. J Invest Derm 1997; 2: 37–40.
  46. Garcia-Castro M, Bronner-Fraser M. Induction and differentiation of the neural crest. Curr Opin Cell Biol 1999; 11: 695–8.[CrossRef][Medline]
  47. Thaller V, Vrkljan M, Hotujac L, Thakore J. The potential role of hypocortisolism in the pathophysiology of PTSD and psoriasis. Coll Antropol 1999; 23: 611–9.[Medline]
  48. Terui T, Ozawa M, Tagami H. Role of neutrophils in induction of acute inflammation in T-cell-mediated immune dermatosis, psoriasis: a neutrophil-associated inflammation-boosting loop. Exp Dermatol 2000; 9: 1–10.[CrossRef][Medline]
  49. Trepicchio WL, Ozawa M, Walters IB, Kikuchi T, Gilleaudeau P, Bliss JL, Schwertschlag U, Dorner AJ, Krueger JG. Interleukin-11 therapy selectively downregulates type I cytokine proinflammatory pathways in psoriasis lesions. J Clin Invest 1999; 104: 1527–37.[Medline]
  50. Espinoza LR, van Solingen R, Cuellar ML, Angulo J. Insights into the pathogenesis of psoriasis and psoriatic arthritis. Am J Med Sci 1998; 316: 271–6.[CrossRef][Medline]
  51. Nickoloff BJ. The immunologic and genetic basis of psoriasis. Arch Dermatol 1999; 135: 1104–10.[Free Full Text]
  52. Ionescu G, Kiehl R. Plasma catecholamine levels in severe atopic eczema. Allergy 1988; 43: 614–6.[Medline]
  53. Singh LK, Pang X, Alexacos N, Letourneau R, Theoharides TC. Acute immobilization stress triggers skin mast cell degranulation via corticotropin releasing hormone, neurotensin, and substance P: s link to neurogenic skin disorders. Brain Behav Immun 1999; 13: 225–39.[CrossRef][Medline]
  54. Staniek V, Doutremepuich J, Schmitt D, Claudy A, Misery L. Expression of substance P receptors in normal and psoriatic skin. Pathobiology 1999; 67: 51–4.[CrossRef][Medline]



This article has been cited by other articles:


Home page
 Arch DermatolHome page
S. M. Ali, R. T. Brodell, R. Balkrishnan, and S. R. Feldman
Poor Adherence to Treatments: A Fundamental Principle of Dermatology
Arch Dermatol, July 1, 2007; 143(7): 912 - 915.
[Full Text] [PDF]

Home page
 Psychosom. Med.Home page
E. L. Altschuler and R. E. Kast
Bupropion in Psoriasis and Atopic Dermatitis: Decreased Tumor Necrosis Factor-{alpha}?
Psychosom Med, July 1, 2003; 65(4): 719 - 719.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Modell, J. G.
Right arrow Articles by Katholi, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Modell, J. G.
Right arrow Articles by Katholi, C.
Related Collections
Right arrow Consultation Psychiatry
Right arrow Dermatology

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS