Lithium treatment and thyroid dysfunction – data from an inpatient psychiatric department

2016 ◽  
Vol 33 (S1) ◽  
pp. S545-S545
Author(s):  
M. Lázaro ◽  
A. Mota ◽  
A. Moreira ◽  
R. Alves ◽  
M.A. Nobre

IntroductionLithium is among the most effective therapies for bipolar disorder. Lithium treatment may cause hypothyroidism, goiter or to a lesser extent hyperthyroidism, since it can affect several aspects of thyroid functioning. The prevalence of lithium-associated hypothyroidism varies extensively between studies, reaching up to 47%, and affecting more females than males (5:1).ObjectiveDetermine the prevalence of thyroid dysfunction in an acute inpatient psychiatric department dedicated to affective disorders and its association with lithium therapy.AimsTo review the relation between lithium treatment and thyroid dysfunction.MethodsObservational, descriptive and retrospective study with clinical and laboratorial data concerning all inpatient episodes of 2015 in our Psychiatric Department. A non-systematic literature search was performed in PubMed.ResultsThe present study documented a high prevalence of thyroid dysfunction, particularly in women. Most cases were due to either hypothyroidism or subclinical hypothyroidism. Patients treated with lithium were more often under thyroid hormone replacement therapy (levothyroxine).ConclusionsThe evidence that lithium treatment is associated with hypothyroidism is well established and this condition is easily treatable with levothyroxine. This study highlights the importance of baseline screening of thyroid function and regular long-term monitoring in patients treated with lithium.Disclosure of interestThe authors have not supplied their declaration of competing interest.

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jee Hee Yoon ◽  
Ji Yong Park ◽  
A Ram Hong ◽  
Hee Kyung Kim ◽  
Ho-Cheol Kang

Abstract Background Thyroid dysfunction caused by the immune checkpoint inhibitor (ICPI) is common, however mild dysthyroidism could occur easily in cancer patients due to other causes. The aim of this study was to investigate the incidence and clinical course of ICPI-induced hypothyroidism requiring thyroid hormone replacement. Patients and methods We analyzed baseline and follow up thyroid function tests of cancer patients treated with nivolumab between March 2016 and March 2019 at Chonnam University Hwasun Hospital retrospectively. Results Among 265 cancer patients treated with nivolumab therapy, six patients were excluded from the study because they were on thyroid hormone replacement therapy before starting nivolumab therapy. Twenty-one patients (8.1%) newly developed thyroid dysfunction during nivolumab therapy and sixteen patients (6.2%) required thyroid hormone replacement therapy due to drug-induced hypothyroidism. Cancer diagnoses included lung cancer (n=7), renal cell carcinoma (n=4), malignant melanoma (n=2), hepatocellular carcinoma (n=2), and esophageal cancer (n=1). Six patients (37.5%) showed thyrotoxic phase prior to overt hypothyroidism and the others (n=10, 62.5%) revealed hypothyroidism without thyrotoxic phase. Most ICPI-induced hypothyroidism was irreversible, only one patient was able to discontinue thyroid hormone replacement after quitting nivolumab therapy. Conclusion A significant number of patients treated with nivolumab developed ICPI-induced hypothyroidism requiring thyroid hormone replacement and its clinical course was irreversible in most patients.


2021 ◽  
pp. 105477382110381
Author(s):  
Kelly Haskard-Zolnierek ◽  
Courtney Wilson ◽  
Julia Pruin ◽  
Rebecca Deason ◽  
Krista Howard

Individuals with hypothyroidism suffer from symptoms including impairments to cognition (i.e., “brain fog”). Medication can help reduce symptoms of hypothyroidism; however, brain fog may hinder adherence. The aim of this study was to determine if memory impairment and cognitive failures are related to treatment nonadherence in 441 individuals with hypothyroidism. Participants with a diagnosis of hypothyroidism and currently prescribed a thyroid hormone replacement medication were placed in two groups according to adherence level and compared on validated scales assessing impairments to memory and cognition. Results indicated a significant association between treatment nonadherence and self-reported brain fog, represented by greater cognitive and memory impairments. Nonadherent individuals indicated impairments with prospective, retrospective, and short- and long-term memory; and more cognitive failures, compared to adherent individuals. Findings suggest the importance of interventions to enhance adherence for individuals with brain fog, such as encouraging the use of reminders.


2005 ◽  
Vol 49 (3) ◽  
pp. 468-472 ◽  
Author(s):  
Luiz Augusto Casulari ◽  
Fábio Celotti ◽  
Luciana A. Naves ◽  
Lucília Domingues ◽  
Carla Papadia

Long term use of high doses of estrogen and the presence of chronic hyperprolactinemia may, at least in the rat, provoke lesions in the tuberoinfundibular dopaminergic (TIDA) neurons responsible for the control of prolactin (Prl) secretion. This occurrence, which is not yet well documented in humans, may have taken place in a patient on chronic oral hormonal contraceptive (OC) treatment who was seen for primary hypothyroidism, hyperprolactinemia and a pituitary mass. After thyroid hormone replacement, OC withdrawn and bromocriptine treatment, this patient could not maintain normal Prl levels, unless continuously treated with a dopaminergic agonist even when MRI was indicative of a normal situation. Function of TIDA neurons was investigated by TRH test (200µg IV) performed before and after treatment with 25mg carbidopa plus 250mg L-dopa every 4 hours for one day. Basal TSH was normal (3.9µU/mL) whereas basal Prl was high (67.5 ng/mL); both TSH and Prl levels appropriately increased after TRH: peaks 31.8µU/mL and 157.8 ng/mL, respectively. After treatment with carbidopa/L-dopa, basal TSH (1.6µU/mL) and Prl (34ng/mL) decreased and the response to TRH was partially blocked (10.3µU/mL and 61ng/mL, respectively). In spite of a normal response, we discuss the possibility that the persistence of hyperprolactinemia is due to lesion of the TIDA neurons produced by the long term use of high doses of estrogens and by the presence of chronic hyperprolactinemia.


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