LETTER TO THE EDITOR
Year : 2016 | Volume
: 13 | Issue : 3 | Page : 146--147
Autoimmune thyroid disorder and recurrent depression: Clinicians must be aware of the links
Karishma Rupani, Avinash De Sousa, Nilesh Shah
Department of Psychiatry, Lokmanya Tilak Municipal Medical College, Mumbai, Maharashtra, India
Avinash De Sousa
Carmel, 18, St. Francis Road, Off S.V. Road, Santacruz West, Mumbai - 400 054, Maharashtra
|How to cite this article:|
Rupani K, De Sousa A, Shah N. Autoimmune thyroid disorder and recurrent depression: Clinicians must be aware of the links.Thyroid Res Pract 2016;13:146-147
|How to cite this URL:|
Rupani K, De Sousa A, Shah N. Autoimmune thyroid disorder and recurrent depression: Clinicians must be aware of the links. Thyroid Res Pract [serial online] 2016 [cited 2020 Sep 19 ];13:146-147
Available from: http://www.thetrp.net/text.asp?2016/13/3/146/193138
Autoimmune thyroid disorder causing hypothyroidism may be missed by clinicians in routine clinical practice if antibody testing is not carried out.  Hypothyroidism has been positively correlated with a diagnosis of depression, subclinical depression, and depressive features. Patients with hypothyroidism that have depression may take longer to recover, and treatment of the thyroid disorder has a direct putative role in the management of depression as well.  Autoimmune thyroid disorder has been linked to depression and a higher prevalence of both antimicrosomal antibodies (AMAs) and antithyroid peroxidase (TPO) antibodies have been found in patients with depression.  We discuss herewith a case of depression that visited our outpatient department and in the course of routine investigations and assessment was uncovered to be a case of autoimmune thyroid disorder.
A 42-year-old woman presented to the psychiatry outpatient clinic with chief complaints of decreased social interactions with family members over the past 7 months before presentation. She would remain isolated and aloof, stopped pursuing her hobbies and showed signs of inactiveness and lethargy. The relatives mentioned that she became very slow in her daily chores and was unable to complete them like before. She would cry often and expressed a wish to die. There was, however, no suicidal attempt made by the patient. She would feel fatigued and complained of a delay in sleep onset though sleep was not disturbed. This was the fourth such episode in the patient, and it was the first visit to our clinic. The first episode occurred 6 years before presentation without any precipitating factors, and the symptoms were similar to those described above. Psychiatric help was sought in the first episode by a private psychiatrist, and the patient was diagnosed as having major depressive disorder. She was started on escitalopram in a dose of 15 mg per day. She continued treatment for a period of 9 months and stopped medication on her own as she showed over 85% improvement. Her symptoms did not return on stopping the medication. She had a second episode 4 years before the present episode and immediately consulted the same doctor. She was restarted on escitalopram with a maximum dose of 15 mg per day. This time, too she showed over 80% improvement in 4 weeks of treatment. The patient stopped follow-up and medication in 6 months as she was better. In the second episode, she complained of oligomenorrhea that was not treated. A thyroid hormone profile done 4 years back revealed no abnormality. Within 3 weeks of stopping the medication, the patient had a relapse of symptoms with sadness, crying spells, and feeling helpless in addition to her lethargy. This time, she was started on escitalopram and venlafaxine. The patient improved to 50% after 4 weeks and continued treatment for another 10 months.
This time, though compliant with treatment, the patient had a worsening of her symptoms and visited our set up. She had gained 11 kg during the previous year. An endocrinology opinion was sought from our institution, thyroid profile (free T3, T4, TSH levels) was repeated which was normal. The endocrinologist suggested getting serum anti-TPO antibody and AMA tests done. The patient tested positive for both, and it was suggested that the patient is given 25 µg of thyroxine in addition to her psychotropic medications. On follow-up, not only did the sadness abate but also fatigability, poor motivation, and lethargy decreased significantly. Her menstrual cycle was regular, and she lost 6 kg of weight while being able to do her daily chores as well as before. She has been following up and is currently asymptomatic and functioning well. She has been maintained on just escitalopram 15 mg per day and thyroxine in the morning.
Our case highlights the need for screening patients with depression to rule out autoimmune thyroid disorder. Thyroid hormones may at times be reported normal in laboratory investigations and yet autoimmune processes may contribute to subclinical hypothyroidism and subclinical depression. This screening is vital when symptoms do not remit with antidepressant treatment and thyroid profiles are normal while the patient shows subtle signs of hypothyroidism (in our case lethargy, fatigue, weight gain, and menstrual disturbances).  Subclinical hypothyroidism may produce depressive symptoms and cognitive deficits although these tend to be less severe than those produced by overt hypothyroidism. Among patients with subclinical hypothyroidism, the lifetime prevalence of depression in patients is approximately double that of the general population. A lower response rate to antidepressants or antidepressant refractoriness has been observed among patients with subclinical hypothyroidism. They also show a greater likelihood to respond to T3 augmentation as compared to euthyroid depressed patients.  Studies have reported a greater prevalence of antithyroid antibody titers in patients with depression, estimated at 9-25%, compared to the general population rate of approximately 5%. Around 20% of patients with depressive disorder had detectable titers of antithyroid antibodies, a rate considerably higher than the 5-10% observed in the normal population. Each of these 20% patients with symptomless autoimmune thyroiditis had normal baseline serum thyrotropin concentrations and normal thyroid function (as assessed by T4, T3 uptake, and free thyroxine index). These findings support the hypothesis of subtle thyroid dysfunction in a sizable sample of psychiatric patients with prominent depressive symptoms. 
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There are no conflicts of interest.
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