Are autoimmune thyroid dysfunction and depression related?

1998 ◽  
Author(s):  
V. J. M. Pop

2012 ◽  
Vol 27 (1) ◽  
pp. 67-71
Author(s):  
Cristina Jaring ◽  
◽  
Elizabeth Paz-Pacheco ◽  
Cecilia Jimeno ◽  
Ester Gonzales-Penserga ◽  
...  


2001 ◽  
Vol 115 (3) ◽  
pp. 660-663 ◽  
Author(s):  
W. Y. Au ◽  
B. R. Hawkins ◽  
E. Y. T. Chan ◽  
A. K. W. Lie ◽  
A. W. C. Kung ◽  
...  


2020 ◽  
Vol 38 (6) ◽  
pp. 1717-1729
Author(s):  
Ying Zhang ◽  
Francesca Garofano ◽  
Xiaolong Wu ◽  
Matthias Schmid ◽  
Peter Krawitz ◽  
...  

Summary Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), the first immune checkpoint to be targeted clinically, has provided an effective treatment option for various malignancies. However, the clinical advantages associated with CTLA-4 inhibitors can be offset by the potentially severe immune-related adverse events (IRAEs), including autoimmune thyroid dysfunction. To investigate the candidate genes and signaling pathways involving in autoimmune thyroid dysfunction related to anti-CTLA-4 therapy, integrated differentially expressed genes (DEGs) were extracted from the intersection of genes from Gene Expression Omnibus (GEO) datasets and text mining. The functional enrichment was performed by gene ontology (GO) annotation and Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis. Protein-protein interaction (PPI) network, module enrichment, and hub gene identification were constructed and visualized by the online Search Tool for the Retrieval of Interacting Genes (STRING) and Cytoscape software. A total of 22 and 17 integrated human DEGs in hypothyroidism and hyperthyroidism group related to anti-CTLA-4 therapy were identified, respectively. Functional enrichment analysis revealed 24 GO terms and 1 KEGG pathways in the hypothyroid group and 21 GO terms and 2 KEGG pathways in the hyperthyroid group. After PPI network construction, the top five hub genes associated with hypothyroidism were extracted, including ALB, MAPK1, SPP1, PPARG, and MIF, whereas those associated with hyperthyroidism were ALB, FCGR2B, CD44, LCN2, and CD74. The identification of the candidate key genes and enriched signaling pathways provides potential biomarkers for autoimmune thyroid dysfunction related to anti-CTLA-4 therapy and might contribute to the future diagnosis and management of IRAEs for cancer patients.





1998 ◽  
Vol 83 (9) ◽  
pp. 3194-3197 ◽  
Author(s):  
Victor J. Pop ◽  
Luc H. Maartens ◽  
Geraline Leusink ◽  
Maarten J. van Son ◽  
Andre A. Knottnerus ◽  
...  


1984 ◽  
Vol 58 (4) ◽  
pp. 681-687 ◽  
Author(s):  
ROLF JANSSON ◽  
SVERKER BERNANDER ◽  
ANDERS KARLSSON ◽  
KLAS LEVIN ◽  
GÖRAN NILSSON


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A919-A919
Author(s):  
Rebecca Scott ◽  
Emily Cornish ◽  
Daivd Williams

Abstract Introduction: Alemtuzumab is a monoclonal antibody that improves outcomes in patients with relapsing-remitting multiple sclerosis. It binds to CD52 and causes a profound depletion of B and T lymphocytes. Autoreactive T cells often form as the immune system repopulates, causing autoimmune thyroid dysfunction in approximately 35% of patients. Alemtuzumab has been associated with new-onset hyperthyroidism during a subsequent pregnancy. Here, we present the first two cases of alemtuzumab-induced hypothyroidism diagnosed in pregnancy. Diagnosing and treating de novo thyroid dysfunction in pregnancy is essential for optimal fetal development and maternal wellbeing. Clinical Cases: Case A: A 28-year-old woman conceived 26 months after alemtuzumab therapy. Prior to pregnancy, routine TFTs showed euthyroidism. At 17 weeks’ gestation she presented with fatigue, and blood tests confirmed overt hypothyroidism (TSH >100mIU/L (<4IU/L), fT4 3.7pmol/L (9-15pmol/L)). TRABs were positive. She was treated with levothyroxine, and TFTs normalised by 38 weeks’ gestation. Serial fetal ultrasounds showed constant growth velocity and no fetal goitre or tachycardia. The baby was born at term with birthweight on the 30th centile. On day 5 postpartum, the baby had a normal TSH of 3.1mIU/l (0.27-4.20mIU/l) but elevated fT4 of 31.5pmol/L (12-22pmol/L), which fell spontaneously to 22.0pmol/L by day 11. Case B: A 37-year-old woman conceived 19 months after alemtuzumab therapy. Prior to pregnancy, routine TFTs had been within normal limits. However at 5 weeks’ gestation, blood tests showed overt hypothyroidism (TSH 47.9mIU/L (<4iU/L)), fT4 8.8pmol/l (10-16pmol/L)). Her only symptom was fatigue. TRABs were elevated. She was treated with levothyroxine, and TFTs normalised by 16 weeks’ gestation. Serial fetal ultrasound scans showed constant growth velocity and no fetal goitre or tachycardia. The baby was born at term with birthweight on the 25th centile. On day 1 postpartum, the baby had a normal fT4 (16.5pmol/l)but elevated TSH 13.02mIU/L, which normalised spontaneously by day 11 tp 1/64mIU/l. Conclusion: To optimise pregnancy outcomes, we recommend that women previously treated with alemtuzumab should be screened monthly for thyroid dysfunction during a subsequent pregnancy. The neonatal team should be alert to transient neonatal thyroid dysfunction, which, like spontaneous alloimmune neonatal thyroid disease, appears to settle spontaneously. References: Garrahy et al. JCEM, 2019, 104 (9), 3624-3625Thakar et al. JCEM 2019, 104 (9), 3626-3627



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