Can Quetiapine Induced Hypothyroidism be Reversible?

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
V. Kontaxakis ◽  
D. Karaiskos ◽  
B. Havaki-Kontaxaki ◽  
D. Skourides ◽  
P. Ferentinos ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Thyroid Dysfunction ◽  
Reference Range ◽  
Case Reports ◽  
Drug Discontinuation ◽  
Thyroid Function Tests ◽  
Antipsychotic Therapy ◽  
Positive History ◽  
Rare Side Effect ◽  
History Of

Objective:Quetiapine induced hypothyroidism is a rare side effect requiring either drug discontinuation or initiation of thyroid replacement therapy. We highlight the potential reversibility of quetiapine induced hypothyroidism in two such cases.Methods:Two case reports.Results:Case 1.Quetiapine (200mg/day) was initiated to a psychotic female patient due to exaggeration of positive symptomatology. Although her thyroid function tests (TFTs) upon admission were normal after a month significant decreases in T3 and T4 level and an elevation in TSH was observed. 45 days later the TFT returned to normal, although she remained on quetiapine. Case 2. Quetiapine (300mg/daily) was prescribed to a bipolar male patient due to a mixed affective episode with a very good response. Despite his normal admission TFTs, three weeks later a decrease in total T4 and a marked increase in TSH was observed .45 days later, although no measures were taken, TFTs returned within reference range.Conclusions:These are the first cases reporting reversibility of quetiapine induced hypothyroidism. TFTs alterations are dose related, relatively slight and linked to a positive history of thyroid abnormality. Our patients did not fulfil any of these criteria. Besides, hypothyroidism resolved although the antipsychotic therapy was continued and no thyroid replacement therapy was given. We suggest a careful thyroid monitoring for patients initiating quetiapine. However, physicians should wait in cases of thyroid dysfunction, since thyroid dysregulation may soon be resolved.

scholarly journals Overt Hypothyroidism Induced by Prolonged Therapy With Imatinib

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A945-A946
Author(s):  
Ally W Wang ◽  
Emily V Nosova
Keyword(s):  
Tyrosine Kinase ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Case Reports ◽  
Myelogenous Leukemia ◽  
Prolonged Treatment ◽  
Overt Hypothyroidism ◽  
Imatinib Treatment ◽  
Thyroid Function Tests ◽  
History Of

Abstract Background: Imatinib, a tyrosine kinase inhibitor (TKI), is commonly used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors. TKI-induced thyroid dysfunction is recognized as an adverse class effect with most cases occurring between six to twelve months after treatment initiation. Clinical Case: 76-year-old man with hypertension and CML on Imatinib that had been started twenty months prior was admitted for confusion. The patient also reported constipation, cold intolerance, and weight gain despite no change in diet, appetite, or physical activity. On evaluation, his responses to questioning were noticeably delayed, however he was not lethargic. His vital signs were normal and he was otherwise euthyroid on physical exam. He had no known history of thyroid dysfunction. Labs showed a TSH of 94.7 (0.4 - 4.2 uIU/mL), Free T4 0.4 (0.8 - 1.5 ng/dL), and Total T3 30 (87 - 178 ng/dL). Thyroglobulin antibody was 1016 (0.0 - 4.1 U/mL) and TPO antibody was >2000 (0.0 - 5.6 IU/mL). A TSH checked two months before admission was 1.1. Antibody levels had not been checked previously. Thyroid ultrasound demonstrated a hyperemic and heterogeneous thyroid, consistent with thyroiditis. Levothyroxine at a dose of 50 mcg daily was advised, due to patient’s advanced age as well as history of arrhythmia. The patient’s confusion resolved on hospital day three. Repeat thyroid function tests will be checked four to six weeks after Levothyroxine initiation. Discussion: As a class, tyrosine kinase inhibitors are known to cause thyroid dysfunction with the most common medication being Sunitinib. Data related to the effects of thyroid function during Imatinib treatment are limited. Previous cases of Imatinib-induced thyroid dysfunction report only hypothyroidism in thyroidectomized patients and no clinically significant change in thyroid function among patients who were euthyroid prior to therapy initiation. Our case reports a patient with no prior thyroidectomy who developed overt hypothyroidism while on Imatinib for nearly two years. The mechanism for TKI-induced thyroid dysfunction has not been elucidated. Due to relatively acute onset and markedly positive TPO and thyroglobulin antibodies, we suspect that TKI may alter HLA recognition on thyroid follicular cells, thereby inducing autoimmunity. Our case showcases the need to maintain awareness and continuous surveillance for thyroid dysfunction when patients are on long term TKI as overt hypothyroidism may be induced by prolonged treatment.

scholarly journals Clozapine-induced stuttering in the absence of known risk factors: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Florence Jaguga
Keyword(s):  
Risk Factors ◽  
Family History ◽  
Side Effect ◽  
Case Reports ◽  
Extrapyramidal Symptoms ◽  
Prior History ◽  
Case Presentation ◽  
Rare Side Effect ◽  
History Of ◽  
Electrophysiological Findings

Abstract Background Stuttering is a rare side effect of clozapine. It has been shown to occur in the presence of one or more factors such as abnormal electrophysiological findings and seizures, extrapyramidal symptoms, brain pathology, and a family history of stuttering. Few case reports have documented the occurrence of clozapine-induced stuttering in the absence of these risk factors. Case presentation A 29-year-old African male on clozapine for treatment-resistant schizophrenia presented with stuttering at a dosage of 400 mg/day that resolved with dose reduction. Electroencephalogram findings were normal, and there was no clinical evidence of seizures. The patient had no prior history or family history of stuttering, had a normal neurological examination, and showed no signs of extrapyramidal symptoms. Conclusion Clinicians ought to be aware of stuttering as a side effect of clozapine, even in the absence of known risk factors. Further research should investigate the pathophysiology of clozapine-induced stuttering.

scholarly journals SWEET SYNDROME AND HASHIMOTO THYROIDITIS: A CASE REPORT AND REVIEW OF THE LITERATURE

2020 ◽  
Vol 6 (4) ◽  
pp. e179-e182
Author(s):  
Jacob Goodwin ◽  
Samuel Ives ◽  
Hiba Hashmi
Keyword(s):  
Thyroid Dysfunction ◽  
Case Reports ◽  
Hashimoto Thyroiditis ◽  
Skin Lesions ◽  
Thyroid Stimulating Hormone ◽  
Disease Stage ◽  
Thyroid Peroxidase ◽  
Thyroid Function Tests ◽  
Sweet Syndrome ◽  
Pubmed Database

Objective: Sweet syndrome (SS) is characterized by an inflammatory rash that has been associated with a number of drugs and malignant, inflammatory, and infectious conditions. Rare accounts of Hashimoto thyroiditis (HT) presenting with SS exist in the literature. HT is usually identified after the onset of skin lesions and without signs of overt thyroid dysfunction, and the stage of thyroid disease stage at presentation is variable. Methods: A search of the PubMed database was performed using search criteria involving combinations of “Sweet syndrome” and “Hashimoto thyroiditis,” “autoimmune thyroiditis,” or “thyroiditis,” and the search was filtered for clinical case reports. Five case reports were identified to describe the coexistence of Sweet syndrome and Hashimoto thyroiditis, and full-text versions of these reports were obtained and reviewed. Of note, cases involving subacute or other types of thyroiditis were excluded. Results: A 57-year-old man presented with painful eruptions on his hands; he was initially treated with antibiotics for presumed cellulitis without relief. Skin biopsy later confirmed SS and subsequent workup identified underlying HT with an elevated thyroid-stimulating hormone of 19.24 mU/L (normal, 0.30 to 4.30 mU/L) and positive thyroid peroxidase (TPO) antibody at 236.4 IU/mL. Conclusion: Thyroid function tests should be universally evaluated in the workup of SS, and it may be appropriate to test for TPO antibodies even in the absence of objective thyroid dysfunction. Both SS and HT show immune diathesis, so further work should be undertaken to establish whether a common immunologic trigger exists.

scholarly journals MON-499 Nivolumab-Induced Hypothyroidism Is Irreversible in Most Patients

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jee Hee Yoon ◽  
Ji Yong Park ◽  
A Ram Hong ◽  
Hee Kyung Kim ◽  
Ho-Cheol Kang
Keyword(s):  
Hormone Replacement Therapy ◽  
Thyroid Hormone ◽  
Replacement Therapy ◽  
Cancer Patients ◽  
Thyroid Dysfunction ◽  
Clinical Course ◽  
Hormone Replacement ◽  
Thyroid Function Tests ◽  
Thyroid Hormone Replacement ◽  
Thyroid Hormone Replacement Therapy

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.

scholarly journals Spurious T3 Thyrotoxicosis Unmasking Multiple Myeloma

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Marianna Antonopoulou ◽  
Arnold Silverberg
Keyword(s):  
Multiple Myeloma ◽  
Reference Range ◽  
Laboratory Data ◽  
Thyroid Function Tests ◽  
Laboratory Studies ◽  
Monoclonal Immunoglobulin ◽  
Monoclonal Immunoglobulins ◽  
History Of ◽  
Spurious Results ◽  
Assay Interference

Objective. To document a case of spurious T3 thyrotoxicosis in a 54-year-old woman.Methods. We present the diagnostic approach of a patient with euthyroid hypertri-iodothyronemia.Results. A 54-year-old, clinically euthyroid woman without personal or family history of thyroid disease referred to endocrinology for possible T3 thyrotoxicosis, after thyroid function tests revealed total T3 > 800 ng/dL (reference range 60–181), normal TSH, and T4. The laboratory data were not compatible with the clinical picture, so thyroid binding globulin abnormalities were suspected. Additional laboratory studies confirmed the diagnosis of multiple myeloma.Conclusion. Monoclonal gammopathy is characterized by the presence of a monoclonal immunoglobulin in the serum or urine, occurring in multiple myeloma, and can cause assay interference and spurious results. We identify a newly recognized cause of euthyroid hypertri-iodothyronemia, due to binding of T3 to monoclonal immunoglobulins in the setting of multiple myeloma. Our case is the only one to date suggesting that monoclonal immunoglobulins from multiple myeloma may exhibit binding to T3 only.

scholarly journals Urinary Incontinence due to Overactive Detrusor Muscle: A Rare Side Effect of Venlafaxine

2015 ◽  
Vol 2015 ◽  
pp. 1-2 ◽  
Author(s):  
Vithyalakshmi Selvaraj ◽  
Palanikumar Gunasekar ◽  
Suneel Kumar ◽  
Imad Alsakaf
Keyword(s):  
Major Depressive Disorder ◽  
Urinary Incontinence ◽  
Case Reports ◽  
Prostatic Hyperplasia ◽  
Prior History ◽  
Detrusor Muscle ◽  
Major Depressive ◽  
Overactive Detrusor ◽  
Rare Side Effect ◽  
History Of

We report a case of reemergence of urinary incontinence (UI) in a patient with benign prostatic hyperplasia (BPH) after starting treatment with venlafaxine who was stabilized on tamsulosin and finasteride for about 6 years. A 66-year-old Caucasian male with prior history of major depressive disorder developed UI within a week of starting venlafaxine 75 mg per day. He described symptoms in the form of involuntary leakage of urine both during the day and at night. His symptoms of UI resolved after stopping the venlafaxine. To the best of our knowledge, there are only four case reports of venlafaxine induced urinary incontinence which have been published.

scholarly journals Pretibial myxedema in a euthyroid patient: a case report

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Rediet Ambachew ◽  
Tizita Yosef ◽  
Aklilu M. Gebremariam ◽  
Lishan Demere ◽  
Theodros Aberra ◽  
...  
Keyword(s):  
Case Reports ◽  
Skin Lesions ◽  
Thyroid Function Tests ◽  
Thyroid Disorder ◽  
Rare Presentation ◽  
Case Presentation ◽  
Normal Thyroid Function ◽  
History Of ◽  
Euthyroid Patient ◽  
Pretibial Myxedema

Abstract Background Pretibial myxedema also known as localized myxedema, thyroid dermopathy, or infiltrative dermopathy and rarely as localized mucinosis is an infrequent manifestation of Graves’ disease. It can appear before, during, or after the thyrotoxic state. Euthyroid pretibial myxedema is a rare presentation with few case reports in the literature. This case highlights the importance of considering pretibial myxedema when characteristic skin lesions are observed in a euthyroid patient. Case presentation A 72-year old male Ethiopian patient with a very rare presentation of biopsy-proven pretibial myxedema in a euthyroid state without history of thyroid disease and absence of thyroid autoimmune markers. Resolution of skin lesion was achieved after topical corticosteroid application. Conclusion Absence of history of thyroid disorder and normal thyroid function tests should not exclude the diagnosis of pretibial myxedema.

scholarly journals Association of thyroid dysfunction with abnormal uterine bleeding

2018 ◽  
Vol 7 (6) ◽  
pp. 2388
Author(s):  
Lakshmi Manjeera M. ◽  
Prabhneet Kaur
Keyword(s):  
Thyroid Dysfunction ◽  
Endometrial Thickness ◽  
Abnormal Uterine Bleeding ◽  
Uterine Bleeding ◽  
Thyroid Function Tests ◽  
Medical College ◽  
History Of ◽  
Hormonal Steroids ◽  
Thyroid Abnormalities ◽  
Rule Out

Background: Abnormal uterine bleeding is a common complaint for women being referred to the gynaecologist and is associated with an array of symptoms. The objective of this study was to detect association of thyroid dysfunction in patients with menstrual irregularitiesMethods: This non-interventional prospective study was done over a period of one and half years in a private medical college in Mangalore. All patients in age group of 15-55 years who presented with history of menstrual disturbances were enrolled and evaluated in the study. Patients with structural causes of AUB or using IUCDs or hormonal steroids were excluded. Total of 85 patients were hence evaluated. These 85 patients were subjected to routine investigations like Hb, BT, CT and platelets (to rule out coagulation defects) along with TSH, T3, T4 estimation. Ultrasound abdomen and pelvis with endometrial thickness was done to rule out structural causes.Results: The most common menstrual disturbance was menorrhagia (47 patients: 55.3%). Thyroid abnormalities were found in 29 of the 85 patients with AUB (34.11%). Of the 29 patients with thyroid dysfunction, 24 were hypothyroid and 5 patients were found to be hyperthyroid.Conclusions: Thyroid abnormalities are frequently associated with menstrual irregularities. Hence Thyroid Function Tests are extremely valuable in patients with provisional diagnosis of AUB and should be made mandatory to avoid unnecessary hormonal or surgical treatment in such patients.

scholarly journals SAT-477 Melanoma Treated with Pembrolizumab Leading to Thyroiditis and Subsequent Hypothyroidism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Heather Fishel
Keyword(s):  
Thyroid Function ◽  
T Cell Activation ◽  
Thyroid Dysfunction ◽  
Subsequent Development ◽  
Thyroid Function Tests ◽  
Free T4 ◽  
Specific Patient ◽  
Normal Thyroid ◽  
Free T3 ◽  
History Of

Abstract Background: Pembrolizumab (PD-1) is an immune checkpoint inhibitor used for treating melanoma and has been associated endocrine immune-related adverse events. Case Presentation: 76-year-old Caucasian male presented for evaluation of abnormal thyroid labs. Significant co-morbidities included recurrent melanoma, heart failure, atrial fibrillation, coronary artery disease, type 2 diabetes, hypertension. Patient’s melanoma was being treated with Pembrolizumab. Further history revealed no family/personal history of thyroid disease but a history of mouth cancer treated with radiation over 30 years ago. He denied any recent glucocorticoid or biotin use. Symptoms included worsening fatigue, weight loss, and diarrhea. He was afebrile and vitally stable. Physical exam was unremarkable. Prior to this year, patient had normal thyroid labs. Recent thyroid labs showed TSH of 0.01 uIU/mL (normal 0.34-4.94 uIU/mL), confirmed with repeat labs a week later (TSH: < 0.01, Free T4: 2.23 ng/dL, normal Free T4: 0.7-1.48 ng/dL). There was a high suspicion that these labs were related to Pembrolizumab, but other etiologies were evaluated. Completed thyroid uptake and scan showed no evidence of increased activity (4-hour uptake: 1.6%, 24-hour update: 1.2%). Repeat thyroid labs indicated recovering thyroid function with a TSH: 0.14 uIU/mL, Free T4: 0.49 ng/dL, Free T3: 1.5 pg/mL (normal Free T3 2.3-4.2 pg/mL), TSI: 96% (normal < 140%), TPO Ab: 111 IU/mL (normal TPO Ab < 9 IU/mL). One month later thyroid tests resulted as TSH: 72.81 uIU/mL, Free T4: < 0.40. He was started on levothyroxine, which was titrated over several weeks. Discussion: Pembrolizumab (PD-1) is an IgG4 programmed cell death 1-directed monoclonal antibody, whose mechanism of action is to inhibit cancer cells ability impede T-cell activation. However, because of this mechanism, some T-cells, will remain activated, leading to autoimmune diseases. PD-1 has been associated with thyroid dysfunction, with an incidence rate as high as 14-20%. The clinical presentation varies from isolated thyrotoxicosis to overt hypothyroidism. In our patient, he developed thyrotoxicosis with subsequent development of hypothyroidism. Generally, the timing of thyroid dysfunction after the initiation of PD-1 ranges from 3 to 40 weeks, with the median onset at week 6. Baseline TSH and free T4 should be obtained with rechecking of these labs monthly for the first 6 months. For patients who present with thyrotoxicosis, Grave’s disease should be ruled out, and initial treatment should include beta-blockers. Hypothyroidism should be treated with levothyroxine with titration to normal thyroid function tests. What remains to be determined is the mechanism in which PD-1 causes thyroid dysfunction and if specific patient characteristics, such as thyroid antibodies, can be used to risk stratify the likelihood of a patient developing thyroid dysfunction.

Dynamics of immune-mediated thyroid dysfunction in patients with advanced renal cell carcinoma receiving checkpoint inhibitor therapy.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e16071-e16071
Author(s):  
Juan Carlos Osorio ◽  
Sujata Patil ◽  
Devyn Taylor Coskey ◽  
Maria Isabel Carlo ◽  
Darren R. Feldman ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Replacement Therapy ◽  
Median Time ◽  
Thyroid Function ◽  
Renal Cell ◽  
Thyroid Dysfunction ◽  
Objective Response ◽  
Cancer Center ◽  
Thyroid Function Tests

e16071 Background: Checkpoint inhibitors (CPI) are quickly gaining relevance in the management of metastatic renal cell carcinoma (RCC). Treatment is generally well tolerated, but immune-induced thyroid dysfunction (TD) is reported in up to 10% of patients (pts) across trials. The dynamics of this phenomenon are undefined; hence there are no proposed standards for endocrine surveillance on therapy. Here we report on a cohort of RCC pts treated with CPI at Memorial Sloan Kettering Cancer Center with serial prospective assessment of thyroid function on therapy. Methods: Thyroid function tests (TFT) were assessed at baseline and serially on therapy. We recorded trends for hyper- and hypothyroidism and determined median time to development of TD by standard statistical methods. T4 replacement therapy was investigated by individual chart review. The association of TD with outcomes on CPI therapy was assessed by non-parametric tests. Results: Of 59 pts with serial TFT assessment, 20 were hypothyroid and 39 were euthyroid at baseline. 50% of previously hypothyroid pts required adjustment of T4 dosage. Thirteen of 39 euthyroid pts (36%) developed new TD requiring thyroid replacement. TD occurred early (median time to onset: 1.4 months, range 0.9-9.6), and in six of the 13 pts (46%), transient thyroiditis preceded hypothyroidism. None of the pts with thyroiditis required treatment, and the median duration from onset of thyroiditis to development of hypothyroidism was 1.5 months (range 0.7-2.8). All pts with hypothyroidism required replacement therapy; none required discontinuation of immunotherapy due to TD. TD was not associated with difference in objective response rate (fisher’s exact, p = 0.163), regression in target lesions (wilcoxon rank-sum, p = 0.135), or PFS (log rank p = 0.8214). Conclusions: TD is common in RCC pts receiving CPI therapy. In this cohort, onset of TD was early, thyroiditis was always transient, and no new cases were detected beyond 10 months. Confirming these findings in larger cohorts will provide meaningful data to guide management of TD when using this new class of agents outside of clinical trials.

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