Lymphocyte proliferation among major depressive and dysthymic patients with typical or atypical features.
BACKGROUND
Depressive illness may be associated with immune and cytokine alterations. However, data are unavailable concerning functional immune changes associated with chronic, low-grade depression (dysthymia). Moreover, the contribution of the neurovegetative features of depression (e.g., altered sleep, eating) to the immune alterations remains to be determined.


METHODS
Mitogen-stimulated cell proliferation was assessed in major depressive and dysthymic patients exhibiting either typical or atypical features. In a subset of patients, lymphocyte proliferation was also assessed before and after pharmacotherapy to determine whether alleviation of symptoms would be accompanied by normalization of immune functioning.


RESULTS
Lymphocyte proliferation was reduced to a greater extent among dysthymic than among major depressive patients. Among dysthymic patients reduced cell proliferation was evident irrespective of symptom typicality; however, among major depressive patients the contribution of neurovegetative features varied with the specific mitogen used. Symptom alleviation following antidepressant treatment was not accompanied by normalization of cell proliferation.


CONCLUSIONS
Patients received 12 weeks of antidepressant treatment, and more sustained therapy may be required for normalization of immune activity. As well, conclusions concerning normalization of immune functioning in drug-treated major depressive patients requires that a greater number of patients be assessed.


CONCLUSIONS
As the immune variations were more pronounced in dysthymia than in major depression, chronicity of illness may be a pertinent factor in promoting immune disturbances. This does not exclude the possibility that depression is associated with immune activation, which then provokes suppression of other aspects of immunity. As well, it is conceivable that immune alterations indirectly contribute to the symptoms accompanying depressive state, although it does not appear that variations of lymphocyte proliferation are associated with neurovegetative status.
Zaharia
M D
MD
Institute of Neuroscience, Carleton University, Ottawa, Canada.
Ravindran
A V
AV
Griffiths
J
J
Merali
Z
Z
Anisman
H
H
D000328:Adult; D018687:Antidepressive Agents, Second-Generation / Q000009:adverse effects / Q000627:therapeutic use*; D003511:Cyclohexanols / Q000009:adverse effects / Q000627:therapeutic use; D003865:Major Depressive Disorder / Q000175:diagnosis / Q000188:drug therapy / Q000276:immunology*; D019263:Dysthymic Disorder / Q000175:diagnosis / Q000188:drug therapy / Q000276:immunology*; D005260:Female; D005473:Fluoxetine / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects / Q000276:immunology; D008213:Lymphocyte Activation / Q000187:drug effects / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D017374:Paroxetine / Q000009:adverse effects / Q000627:therapeutic use; D010555:Personality Inventory; D020280:Sertraline / Q000009:adverse effects / Q000627:therapeutic use; D000069470:Venlafaxine Hydrochloride
D018687:Antidepressive Agents, Second-Generation; D003511:Cyclohexanols; D005473:Fluoxetine; D017374:Paroxetine; D000069470:Venlafaxine Hydrochloride; D020280:Sertraline