Antidepressant therapy. A possible cause of atypical cutaneous lymphoid hyperplasia

Crowson, A. Neil

doi:10.1001/archderm.131.8.925

Cited by 44 publications

(31 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Immune activation may be associated with mood disorders, since inflammatory cytokines have been shown to alter monoamine turnover, decrease activity of presynaptic serotonergic neurons, and indirectly, even activate serotonin reuptake from the synaptic cleft [23]. Indeed, antidepressant therapy has been shown to be associated with an immunomodulatory effect [24]. A report has recently shown that desipramine and fluoxetine reduce the inflammatory reaction in two animal models of human diseases: ovalbumin-sensitized rats and LPS murine model of autoimmunity.…”

Section: Discussionmentioning

confidence: 99%

Evidence for an inhibitory immunomodulatory effect of selected antidepressants on rat splenocytes: Possible relevance to depression and hyperactive-immune disorders

Taler

Bar

Korob

et al. 2008

International Immunopharmacology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Evidence for an inhibitory immunomodulatory effect of selected antidepressants on rat splenocytes: Possible relevance to depression and hyperactive-immune disorders

Taler

Bar

Korob

et al. 2008

International Immunopharmacology

View full text Add to dashboard Cite

“…For example, Reed and Glick [14] have reported a reactivation of herpes simplex virus in several patients being treated chronically with fluoxetine for the treatment of major depression. Similarly, Crowson and Magro [15] reported that patients developed cutaneous pseudolymphoma lesions following initiation of chronic fluoxetine therapy. Both of these conditions resolved with the discontinuation of fluoxetine treatment [14,15].…”

Section: Introductionmentioning

confidence: 84%

“…Similarly, Crowson and Magro [15] reported that patients developed cutaneous pseudolymphoma lesions following initiation of chronic fluoxetine therapy. Both of these conditions resolved with the discontinuation of fluoxetine treatment [14,15]. Therefore, the effect of antidepressant therapy, including the SSRIs, on immune cell function in patients or in animal models of depression is very complex and potentially suppressive.…”

Section: Introductionmentioning

confidence: 84%

Specific Serotonin Reuptake Inhibitor-Induced Decreases in Lymphocyte Activity Require Endogenous Serotonin Release

Pellegrino

Bayer

2000

Neuroimmunomodulation

View full text Add to dashboard Cite

Objectives: We have previously reported that acute administration of the specific serotonin reuptake inhibitor (SSRI), fluoxetine, resulted in a decrease in mitogen-induced blood lymphocyte proliferation. The present studies further examine the specificity of this response to serotonin reuptake systems and the potential role of endogenous serotonin in mediating these effects. Methods: Male Sprague-Dawley rats were treated intraperitoneally with the SSRIs, fluoxetine (6–10 mg/kg) or sertraline (20 mg/kg), dopamine and norepinephrine reuptake inhibitors, GBR 12909 and desipramine, respectively (6 mg/kg) or the serotonin precursor, 5-hydoxytryptophan (5-HTP, 50 mg/kg) 2 h prior to sacrifice. The serotonin-depleting agents, p-chlorophenylalanine (PCPA, 2 × 200 mg/kg) or the serotonin-lesioning agent, p-chloroamphetamine (PCA, 2 × 10 mg/kg) were administered intraperitoneally 5–7 days prior to fluoxetine (10 mg/kg) administration. Results: Unlike the SSRIs, which significantly suppressed lymphocyte proliferation responses, selective norepinephrine or dopamine reuptake inhibition had no effect on lymphocyte proliferation. Elevation of extracellular serotonin levels with the serotonin precursor, 5-HTP, resulted in a similar decrease in lymphocyte proliferation as that seen with SSRI administration. Conversely, decreases in endogenous serotonin following PCA or PCPA treatment prevented the fluoxetine-induced decreases in lymphocyte proliferation. Conclusions: These results suggest that decreases in mitogen-induced lymphocyte proliferation following acute fluoxetine administration were due to elevations in extracellular serotonin following reuptake inhibition.

show abstract

“…Previous experimental and clinical data provided by other authors lead to conflicting hypotheses (Mathews 1995;Storch 1996) about the effects of antidepressants on cancer promotion and growth. Regarding selective serotonin reuptake inhibitor (SSRI) antidepressants, fluoxetine was reported to be both a tumor promoter (Brandes and Cheang 1993;Crowson and Magro 1995) and an antineoplastic agent (Bendele et al 1992;Abdul et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Effects of nefazodone on the development of experimentally induced tumors in stressed rodents

et al. 2004

View full text Add to dashboard Cite

show abstract

Antidepressant therapy. A possible cause of atypical cutaneous lymphoid hyperplasia

Cited by 44 publications

References 0 publications

Evidence for an inhibitory immunomodulatory effect of selected antidepressants on rat splenocytes: Possible relevance to depression and hyperactive-immune disorders

Evidence for an inhibitory immunomodulatory effect of selected antidepressants on rat splenocytes: Possible relevance to depression and hyperactive-immune disorders

Specific Serotonin Reuptake Inhibitor-Induced Decreases in Lymphocyte Activity Require Endogenous Serotonin Release

Effects of nefazodone on the development of experimentally induced tumors in stressed rodents

Contact Info

Product

Resources

About