Status message

Not the entire site translated, but only to "Journal"

Dynamics of Thyroid Axis Hormone Levels in Patients with Affective Spectrum Disorders During Therapy with Venlafaxine

Moscow Research Institute of Psychiatry – Branch of the V.P. Serbsky National  Medical Research Center of Psychiatry and Narcology of the Ministry of Health of the Russian Federation, Moscow, Russia

SUMMARY:
Background. Scientific literature data confirm the relevance of studying the effect of antidepressants on the functioning of the thyroid axis in patients with affective disorders. At the same time, many aspects of this problem remain poorly understood.
Aim of the study. Clarification of the characteristics of the dynamics of the levels of hormones of the hypothalamic-pituitary-thyroid (HPT) axis in patients with affective disorders during therapy with venlafaxine.
Materials and methods. The study included 72 patients: 24 men and 48 women aged 20 to 55 years (mean age 43.8 ± 14.2 years) with affective spectrum disorders (F31.3; F33.1; F41.2). Therapy was carried out with venlafaxine at a dose of 75–150 mg/day, as a monotherapy. The average daily dosage was 141.16 ± 52.3 mg/day. The studies of thyroid-stimulating hormone (TSH), triiodothyronine (T3), free thyroxine (T4-free) were carried out before the start of therapy, after 14 days and after 28 days of therapy.  
Results. Venlafaxine therapy for 4 weeks was effective in assessing responsiveness (more than 50 % reduction on the HDRS scale) in all patients studied. The baseline values of TSH, T3 and T4 made it possible to ascertain the presence of subclinical hypothyroidism in 8.3 % of patients with bipolar affective disorder (BAD) and in 6.25 % with recurrent depressive disorder (RDD). In patients with bipolar disorder, there was an improvement in the functioning of the GGT axis, as indicated by a significant (p = 0.018) increase in the level of triiodothyronine (T3) by day 28 of therapy, as well as significant negative correlations between TSH and T3 at stages 2 and 3 of the study (r = –0.61, p = 0.0034; r = –0.61; p = 0.0029, respectively), despite slight fluctuations in the direction of decreasing T4 levels in 25 % of patients. In patients with recurrent depressive disorder, by the 14th and 28th days of therapy, the number of patients with a decrease in the levels of peripheral hormones increased against the background of fairly stable TSH indices, which may indicate the presence of a functional hypothyroid state. In patients with anxiety depressive disorder (ADD), by the 14th day, only T4 levels (fluctuations in the reference range) significantly decreased against the background of minor fluctuations in TSH and T3.
Conclusions. The study showed that venlafaxine, in addition to being highly effective, was shown to be safe in terms of its effect on the thyroid axis. This is indicated by the normative indicators of the average values of the hormone HPT axis in the course of therapy. In addition, there was a normalization of elevated background TSH values in patients of all groups. The decrease in the level of peripheral hormones in a number of patients with recurrent depressive disorder may be associated, in all likelihood, with the underlying disease.
CONTACT: Gorobets Lyudmila Nikolaevna, gorobetsln@mail.ru, https://orcid.org/0000-0001-7075-1107
CITATION: Gorobets L.N., Bulanov V.S., Litvinov A.V., Vasilenko L.M., Akhmedova A.A. Dynamics of thyroid axis hormones in patients with affective spectrum disorders during therapy with venlafaxine // Sovrem. ter. psih. rasstrojstv [Current Therapy of Mental Disorders]. – 2021. – No. 2. – Pр. 19–26. – DOI: 10.21265/PSYPH.2021.57.2.003 

CONFLICT OF INTEREST: the authors declare no conflict of interest.
 

It appears your Web browser is not configured to display PDF files. Download adobe Acrobat or click here to download the PDF file.

References: 

1.    Costache A., Riza A.L., Popescu M. et al. TSH and T4 levels in a cohort of depressive patients // Curr Health Sci J. – 2020. – Vol. 46 (2). – Pp. 117–122. – DOI: 10.12865/CHSJ.46.02.03 
2.    Nobis A., Zalewski D., Waszkiewicz N. Peripheral markers of depression // J Clin Med. – 2020. – Vol. 9 (12). – AArt. 3793.  – DOI: 10.3390/jcm9123793
3.    Danilov D.S. Antidepressanty – ingibitory obratnogo zakhvata serotonina i noradrenalina: vzglyad cherez prizmu 30-letnei istorii // Nevrologiya, neiropsikhiatriya, psikhosomatika. – 2018. – Vol. 10 (4). – Pp. 4–12. – DOI: 10.14412/2074-2711-2018-4-4-12
4.    Baumgartner A., Campos-Barros A. Chronic desipramine treatment enhances thyroxine deiodination in rat brain // Psychiatr Res. – 1990. – Vol. 34. – Pp. 217–219.
5.    Comby F., Jambut-Absil A.C., Buxeraud J. et. al. Spectroscopic analysis of charge transfer complex formation between neuroleptics and iodine // Chem Pharm Bull. – 1989. – Vol. 37, no. 1. – Pp. 151–154.
6.    Joffe R. T., Singer W. The effects of tricyclic antidepressants on basal thyroid hormone levels in depressed patients // Pharmacopsychiatry. –1990. – Vol. 23. – Pp. 67–69.
7.    Rousseau A., Comby F., Buxeraud J. et. al. Spectroscopic analysis of charge transfer complex formation and peroxidase inhibition with tricyclic antidepressant drugs: Potential anti-thyroid action // Biol Pharmacol Bull. – 1996. – Vol. 19, no. 5. – Pp. 726–728.
8.    Shelton R.C., Winn S., Ekhatore N. et. al. The effects of antidepressants on the thyroid axis in depression // Biol Psychiatry. – 1993. – Vol. 33. – Pp. 120–126.
9.    Rang H.P., Dale M.M. Pharmacology. 3rd ed. – New York: Churchill Livingstone, 1995. 
10.    Uzbekov M.G., Maximova N.M. The relationship between monoaminergic and hormonal systems and endogenous intoxication in mixed anxiety-depressive disorder // Neurochem J. – 2014. – Vol. 8, no. 4. – Pp. 311–318. 
11.    Atterwill C.K., Catto L.C., Dickens T.A., Heal D.J., Holland C.W. Secretion of TSH and thyroid hormones following treatment of rats with desipramine or ECS // Br. J Pharmacol. – 1988. – Vol. 92. P. 671.
12.    Lyons D.J., Ammari R., Hellysaz A., Broberger C. Serotonin and antidepressant SSRIs inhibit rat neuroendocrine dopamine neurons: Parallel actions in the lactotrophic axis // J Neurosci. – 2016. – Vol. 36 (28). – Pp. 7392–7406. – DOI: 10.1523/JNEUROSCI.4061-15.2016 
13.    Scanlon M.F., Peters J., Foord S. et. al. The clinical relevance of TRH in diagnosis and investigation // Griffiths E.L., Bonnet G.W. (eds.). Thyrotropin-Releasing-Hormone. – New York: Raven Press, 1983. – Pp. 303–314. 
14.    Brady K.T., Anton R.F. The thyroid axis and desipramine treatment in depression // Biol Psychiatry. – 1989. – Vol. 25. – Pp. 703–709.
15.    Morley J.E., Brammer G.L., Sharp B. et. al. Neurotransmitter control of hypothalamic-pituitary-thyroid function in rats // Eur J Pharmacol. – 1981. – Vol. 70. – Pp. 263–271.
16.    Ansseau M., von Frenckell R., Mertens C., de Wilde J., Botte L., Devoitille J.M., Evrard J.L., De Nayer A., Darimont P., Dejaiffe G. et al. Controlled comparison of two doses of milnacipran (F2207) and amitriptyline in major depressive inpatients // Psychopharmacology (Berl). – 1989. – Vol. 98. – Pp. 163–168. 
17.    Gitlin M., Altshuler L.L., Frye M.A. Peripheral thyroid hormones and response to selective serotonin reuptake inhibitors // J Psychiatry Neurosci. – 2004. – Vol. 29, no. 5. – Pp. 383–386.
18.    De Carvalho G.A., Bahls S.C., Boeving A. et al. Effects of selective serotonin reuptake inhibitors on thyroid function in depressed patients with primary hypothyroidism or normal thyroid function // Thyroid. – 2009. – Vol. 19, no. 7. – Pp. 691–697.
19.    Gambi F., De Berardis D., Sepede G. et al. Effect of mirtazapine on thyroid hormones in adult patients with major depression // Int J Immunopathol Pharmacol. – 2005. – Vol. 18, no. 4. – Pp. 737–744.
20.    Eker S.S., Akkaya C., Sarandol A. et al. Effects of various antidepressants on serum thyroid hormone levels in patients with major depressive disorder // Prog Neuropsychopharmacol Biol Psychiatry. – 2008. – Vol. 32, no. 4. – Pp. 955–961.
21.    Gorobets L.N., Pavlova T.A., Dorovskikh I.V. Neiroendokrinnye aspekty patogeneza i psikhofarmakoterapii panicheskogo rasstroistva // Psikhiatriya. – 2016. – № 72 (04). – S. 55–69. 
22.    Häuser W., Petzke F., Üçeyler N., Sommer C. Comparative efficacy and acceptability of amitriptyline, duloxetine and milnacipran in fi bromyalgia syndrome: a systematic review with meta-analysis // Rheumatology (Oxford). – 2011. – Vol. 50, no. 3. – Pp. 532–543.
23.    Kohno T., Kimura M., Sasaki M., Obata H., Amaya F., Saito S. Milnacipran inhibits glutamatergic N-methyl-D-aspartate receptor activity in spinal dorsal horn neurons // Mol Pain. – 2012. – Vol. 8. – P. 45.
24.    Sambunaris A., Bose A., Gommoll C.P., Chen C., Greenberg W.M., Sheehan D.V. A phase III, double-blind, placebo-controlled, fl exibledose study of levomilnacipran extended-release in patients with major depressive disorder // J Clin Psychopharmacol. – 2014. – Vol. 34. – Pp. 47–56.
25.    Hamilton M. A rating scale for depression // Journal of Neurology, Neurosurgery and Psychiatry. – 1960. – Vol. 23. – Pp. 56–62.
26.    Hamilton M. The assessment of anxiety states by rating // Br J Med Psychol. – 1959. – Vol. 32. – Pp. 50–55.
27.    Baikova I.A. Effektivnost' venlaksora (venlafaksina) pri lechenii depressivnykh rasstroistv // Zdravookhranenie. – 2009. – № 4. – S. 41–44.
28.    Maruta N.A., Semikina E. E. Effektivnost' preparata venlaksor pri lechenii depressivnykh rasstroistv // Ukrainskii vestnik psikhonevrologii. – 2007. – Tom 15, vyp. 2 (51). – S. 139–142.
29.    Mosolov S.N., Kostyukova E.G., Gorodnichev A.V. i soavt. Klinicheskaya effektivnost' i perenosimost' preparata venlafaksin (Velaksin) pri lechenii umerennoi i tyazheloi depressii // Trudnyi patsient. – 2007, Noyabr'. – URL: https://t-pacient.ru/articles/6214/ (data obrashcheniya 12.04.2021).
30.    Lenox-Smith A.J., Reynolds A. A double-blind, randomised, placebo controlled study of venlafaxine XL in patients with generalised anxiety disorder in primary care // Br J Gen Pract. – 2003. – Vol. 53. – Pp. 772–777.
31.    Ressler K.J., Nemeroff C.B. Role of serotonergic and noradrenergic systems in the pathophysiology of depression and anxiety disorders // Depression and Anxiety. – 2000. – Vol. 12, Suppl. 1. – Pp. 2–19.
32.    Kasper S. Depression and anxiety – separate or continuum // World J Biol Psychiatry. – 2001. – Vol. 2. – Pp. 162–163. 
33.    Berent D., Zboralski K., Orzechowska A., Gałecki P. Thyroid hormones association with depression severity and clinical outcome in patients with major depressive disorder // Mol Biol Rep. – 2014. – Vol. 41 (4). – Pp. 2419–2425. – DOI: 10.1007/s11033-014-3097-6
34.    Gommoll C.P., Greenberg W.M., Chen C. A randomized, double-blind, placebo-controlled study of fl exible doses of levomilnacipran ER (40-120 mg/day) in patients with major depressive disorder // J Drug Assess. – 2014. – Vol. 3, no. 1. – Pp. 10–19.
35.    Montgomery S.A., Mansuy L., Ruth A., Bose A., Li H., Li D. Effi cacy and safety of levomilnacipran sustained release in moderate to severe major depressive disorder: a randomized, double-blind, placebocontrolled, proof-of-concept study // J Clin Psychiatry. – 2013. – Vol. 74, no. 4. – Pp. 363–369.
36.    Mazo G.E., Gorobets L.N. Strategiya augmentatsii kak odin iz vidov kombinirovannoi terapii u bol'nykh s depressivnymi rasstroistvami (litii i tireoidnye gormony) // Sotsial'naya i klinicheskaya psikhiatriya. – 2020. – T. 30, № 2. C. 52–61.