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: 3.38). 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.

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    • "determination methods ) in the final rates could also be more relevant (Pedersen et al., 2003). In fact, gender and age could influence auto-antibodies in BD-I more than the affective diagnosis, affective state, or medication (Hornig et al., 1999). Thyroid auto-immunity itself appears early in susceptible individuals and has been demonstrated to depend basically on genetic factors (up to 67%) and less on environmental factors (Brix et al., 2004; Hansen et al., 2006) in community pedigrees. "
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    ABSTRACT: Background: Among the biological factors associated with the development and outcomes in Bipolar Disorder Type I (BD-I), previous studies have highlighted the involvement of both thyroid function and/or auto-immunity, proposing a thyroid endophenotype. The objective of this study was to determine the presence of thyroid alterations in BD-I and their first-degree relatives (FDR). Methodology: Unselected, cross-sectional case-control study with parallel analysis of individuals affected by BD-I (239), their FD-R (131), and 108 healthy controls. Thyroidal functional abnormalities (TSH and free T4) and thyroidal antibodies (thyroglobulin and thyroperoxidase antibodies) were studied. Assessments were carried out in parallel. The sample was described using arithmetic means, standard deviations, percentages and ranges. Chi-square, Student-t tests, ANOVA and Pearson correlation coefficients were used when indicated. Results: BD-I on actual and/or ever treated with lithium showed significant thyroidal functional abnormalities as compared to their FD-R and healthy controls. This BD-I subgroup showed a significant greater proportion of subjects suffering from subclinical hypothyroidism (22%). The role of gender/lithium interactions was relevant. The groups did not show differences in terms of positivization of thyroidal antibodies. Limitations: The crosssectional design and the lack of determination of dietary iodine deficiencies and/or thyroidal ecographical controls may be a drawback. Conclusions: The present study supports previous findings on the effect of lithium treatment on thyroidal functional, but did not support previous findings related to a familial association or endophenotype. In addition, the present study did not support a familial aggregation of thyroidal antibodies positivization in pedegrees of BD-I.
    Psychoneuroendocrinology 01/2015; 51. DOI:10.1016/j.psyneuen.2014.09.032 · 4.94 Impact Factor
    • "In contrast, an Italian study did not detect increased TAA in patients with rapid-cycling or non-rapid-cycling bipolar disorders (Bartalena et al., 1990). Also Hornig et al. (1999) did not find in inpatients of a retrospective study a clear association of affective symptoms and TAA, just like an American study in hospitalized patients (Haggerty et al., 1997). "
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    ABSTRACT: Hashimoto’s thyroiditis (HT) is the most frequent cause of hypothyroidism in areas with sufficient iodine intake. While the impact of thyroid function on mood and cognition is well known, only in the recent years, an increasing number of studies report on the association of HT with cognitive and affective disturbances also in the euthyroid state. Recent imaging studies have shown that these impairments are accompanied by altered brain perfusion, in particular, in the frontal lobe and a reduced grey matter density in the left inferior gyrus frontalis. Brain function abnormalities in euthyroid patients with HT may be subtle and only detected by specific testing or even severe as it is the case in the rare neuropsychiatric disorder Hashimoto’s encephalopathy (HE). The good response to glucocorticoids in patients with HE indicates an autoimmune origin. In line with this, the cognitive deficits and the high psycho-social burden in euthyroid HT patients without apparent signs of encephalopathy appear to be associated with anti-thyroid peroxidase auto-antibody (TPO Abs) levels. Though in-vitro studies showing binding of TPO Abs to human cerebellar astrocytes point to a potential direct role of TPO Abs in the pathogenesis of brain abnormalities in HT patients, TPO Abs may function only as a marker of an autoimmune disorder of the central nervous system. In line with this, anti-central nervous system auto-antibodies (CNS Abs) which are markedly increased in patients with HT disturb myelinogenesis in-vitro and, therefore, may impair myelin sheath integrity. In addition, in HT patients, production of monocyte- and T-lymphocyte-derived cytokines is also markedly increased which may negatively affect multiple neurotransmitters and, consequently, diverse brain neurocircuits.
    Brain Behavior and Immunity 10/2014; 41(14). DOI:10.1016/j.bbi.2014.03.008 · 5.89 Impact Factor
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    • "The presence of anti-thyroid antibodies among patients with bipolar disorder was associated with thyroid failure, but not with age, gender, mood state, rapid cycling, or lithium exposure [53]. However, several other controlled studies have not been able to find a higher prevalence of raised antibody tires in bipolar disorder, unrelated to lithium treatment [64, 103, 106]. "
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    ABSTRACT: Accumulating evidence suggests that hypothalamo-pituitary-thyroid (HPT) axis dysfunction is relevant to the pathophysiology and clinical course of bipolar affective disorder. Hypothyroidism, either overt or more commonly subclinical, appears to the commonest abnormality found in bipolar disorder. The prevalence of thyroid dysfunction is also likely to be greater among patients with rapid cycling and other refractory forms of the disorder. Lithium-treatment has potent antithyroid effects and can induce hypothyroidism or exacerbate a preexisting hypothyroid state. Even minor perturbations of the HPT axis may affect the outcome of bipolar disorder, necessitating careful monitoring of thyroid functions of patients on treatment. Supplementation with high dose thyroxine can be considered in some patients with treatment-refractory bipolar disorder. Neurotransmitter, neuroimaging, and genetic studies have begun to provide clues, which could lead to an improved understanding of the thyroid-bipolar disorder connection, and more optimal ways of managing this potentially disabling condition.
    Journal of Thyroid Research 07/2011; 2011(3):306367. DOI:10.4061/2011/306367
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