Article

Autoantibody disturbances in affective disorders: a function of age and gender?

Laboratory for the Study of Emerging Diseases, University of California Irvine, 92697-4292, USA.
Journal of Affective Disorders (Impact Factor: 3.71). 10/1999; 55(1):29-37. DOI: 10.1016/S0165-0327(98)00190-6
Source: PubMed

ABSTRACT Numerous investigators have reported increased autoantibodies to a wide variety of native antigens in patients with affective disorders. However, association of autoimmunity with affective subtypes, mood state, psychotropic medications, age, and gender has not been extensively explored.
The present study assessed 79 bipolar I, 24 bipolar II, and 46 unipolar major depression patients along with 22 healthy, nonpsychiatric controls for the presence of serum antinuclear (ANA), anti-double stranded DNA, antithyroid microsomal, antithyroglobulin, anticardiolipin (ACA) IgM, and ACA IgG antibodies.
Consistent with their higher prevalence of autoimmune disease, women exhibited increased levels of ANA and ACA IgM compared to men. ACA IgG antibody titers also increased significantly with age. Contrary to prior reports of general, overall increases in autoantibodies and specific increases in ANA and antithyroid antibodies in depressed patients, we did not see a significant association between any of the autoantibodies and affective subtype, mood state, or psychotropic medications.
Affective subgroups were heterogeneous with respect to psychotropic medications, affective state, age, and gender in this retrospective analysis. Subgroup sample size was insufficient to determine whether interactions of these clinical variables may have influenced results.
These results suggest that gender and age may have more influence on autoantibodies than affective diagnosis, affective state, or medications.

0 Followers
 · 
81 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: An autoimmune hypothesis has been suggested for a subtype of Obsessive-Compulsive Disorder (OCD) with childhood onset: obsessions, compulsions and/or tics would result from anti-streptococcal antibodies that cross-react with basal ganglia tissue based on molecular mimicry. Consistent with this hypothesis anti-brain antibodies were detected in sera of children with OCD and/or Tourette's syndrome. In the present study, we tested whether adults with OCD have anti-brain antibodies or other antibodies that serve as markers of autoimmunity. Seventy-four DSM-IV OCD (YBOCS> or =16) subjects were recruited and compared to 44 controls with a current Major Depressive Episode for neurological symptoms, ALSO titres, anti-tissue and anti-thyroid antibodies. Anti-brain antibodies were tested by immunohistochemistry and Western blotting methods. The proportion of subjects with tic comorbidity or positive ASLO titre (>200 IU/ml) was significantly greater in OCD than in MDE patients (21.6 vs. 2.3% and 16.3 vs. 2.3%, respectively). No other differences in antibody parameters were found. 4/74 OCD patients (5.4%) and none of the controls resulted positive for anti-brain antibodies, with a band around 50-60 kDa at the Western blot analysis. The methodology used to assess anti-brain antibodies. The majority of adult OCD patients do not seem to have autoimmunity disturbances as compared to a control group. However, a greater percentage of subjects with positive ASLO titres were found among OCD patients. For a small proportion of OCD patients, moreover, autoimmune reactions towards neuronal structures are present although further investigations are needed to demonstrate its etiopathogenetic relevance.
    Journal of Affective Disorders 08/2009; 116(3):192-200. DOI:10.1016/j.jad.2008.11.019 · 3.71 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Thyroid hormones are necessary to the brain development and their absence results into serious cognitive defects. There is some evidence that thyroid hormones’ activity is required in the adult brain for a correct neuronal net orchestration as well. The bonds between mood disorders and thyroid imbalances are reviewed in this paper, the molecular background of these poorly defined boundaries is exposed, along with the putative mechanisms that underlie the antidepressant effect of thyroid hormones in the event of augmentation strategy.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Väitekirja elektroonilisest versioonist puuduvad väitekirja aluseks olevate artiklite täistekstid The purposes of this study were to find associations between depression, depressive symptoms and soluble interleukine- 2 receptor (sIL-2R), tumour necrosis factor-α (TNF-α) and anti thyroid peroxidise auto-antibodies (anti-TPO). We investigated the acute and chronic effects of selective serotonin re-uptake inhibitor, escitalopram, alone and in combination with bupropion on serum levels of interleukin-8 (IL-8), sIL-2R and TNFα in patients with major depression. In addition, we explored whether serum cytokine concentrations and/or anti-TPO positivity can predict treatment response to antidepressants. The levels of TNF-α were lower in currently depressed subjects compared with euthymic subjects in the study cohort. MDD patients with previous antidepressive treatment had significantly lower levels of TNF-α than drug-naïve patients and HC. There were different patterns of changes in the levels of sIL-2R in responders and non-responders to escitalopram treatment. Treatment with escitalopram had no significant effect on the levels of IL-8 and TNF-α. Augmentation of escitalopram treatment with bupropion caused a significant increase in IL-8 serum concentrations during 6 weeks of augmentation therapy. There was no effect on the levels of sIL-2R and TNF-α. The lower baseline TNF-α level was found in the responder group in the escitalopram treatment phase. There was a trend for higher frequency of baseline anti-TPO positive cases in female non-responders to escitalopram monotherapy as compared with responders. There were no significant differences in the levels of thyroid hormones (particularly, total T3, free T3, freeT4, and TSH) between female responders and non-responders. Käesoleva uurimuse eesmärgiks oli seoste leidmine depressiooni, depressiivsete sümptomite ja lahustuva interleukiin-2 retseptori (sIL-2R), tuumor-nekroosfaktor alfa (TNF-α) ning türoid-peroksidaasi autoantikehade vahel (anti-TPO). Me uurisime ka selektiivse serotoniini tagasihaarde inhibiitori, estsitalopraami lühi- ja pikaajalist mõju seerumi interleukiin-8-le (IL-8), sIL-2R-le ja TNFα depressiivsetel patsientidel monoteraapias ja kombinatsioonis bupropiooniga. Lisaks selgitasime, kas seerumi tsütokiinide kontsentratsioon ja/või anti-TPO positiivsus võib ennustada ravivastust antidepressandile. Depressiivsetel patsientidel oli madalam TNF-α tase võrreldes eutüümsete isikutega. Depressioonipatsientidel, kes olid eelnevalt elu jooksul saanud antidepressantravi, oli oluliselt madalam TNF-α tase kui tervetel kontrollisikutel ja eelneva ravita patsientidel. sIL-2R muutused olid erinevad estsitalopraamravile reageerinud ja mittereageerinud patsientidel. Ravi estsitalopraamiga ei mõjutanud oluliselt IL-8 ja TNF-α taset. Estsitalopraami kombineerimine bupropiooniga 6 nädala vältel põhjustas IL-8 taseme tõusu seerumis, sIL-2R ja TNF-α. kontsentratsioonid oluliselt ei muutunud. Ravieelne TNF-α tase oli estsitalopraamravile reageerinud patsientidel madalam kui raviresistentsetel isikutel. Esines tendents, et raviresistentsete naispatsientide hulgas oli enam anti-TPO positiivseid isikuid kui ravile reageerinute hulgas. Naispatsientide ja tervete naiste vahel ei ilmnenud erinevust türoidhormoonide osas (täpsemalt kogu T3, vaba T3, vaba T4 ja TSH).