scholarly journals Simultaneous development of Graves’ disease and type 1 diabetes during anti‐programmed cell death‐1 therapy: A case report

2020 ◽  
Vol 11 (4) ◽  
pp. 1006-1009 ◽  
Author(s):  
Susumu Kurihara ◽  
Yoichi Oikawa ◽  
Ritsuko Nakajima ◽  
Atsushi Satomura ◽  
Ryuhei Tanaka ◽  
...  
2016 ◽  
Vol 53 (5) ◽  
pp. 853-856 ◽  
Author(s):  
Sung Hye Kong ◽  
Seo Young Lee ◽  
Ye Seul Yang ◽  
Tae Min Kim ◽  
Soo Heon Kwak

2019 ◽  
pp. 089719001985092 ◽  
Author(s):  
Kyle A. Farina ◽  
Michael P. Kane

Two Food and Drug Administration-approved programmed cell death-1 (PD-1) inhibitors, nivolumab (Opdivo®), and pembrolizumab (Keytruda®), are indicated for treatment-resistant malignancies. Inhibition of PD-1 also inhibits T-cell peripheral tolerance, enhancing autoimmunity. Various autoimmune conditions have been reported with the use of these agents, including type 1 diabetes mellitus (T1DM). This article reviews literature regarding the development of T1DM in patients treated with PD-1 inhibitors and identifies strategies for the appropriate identification, monitoring, and follow-up of these patients. Published cases of T1DM related to PD-1 inhibitor therapy were identified using PubMed. Eighty-three identified publications were reviewed, of which 37 publications involving 42 cases of anti-PD-1 therapy-induced T1DM were identified. The average age of patients at presentation was 62 years and 59.5% were male. The mean number of PD-1 inhibitor doses received was 5, with a mean time to presentation of 11 weeks. Initial presentation of diabetic ketoacidosis was reported in 69% of cases, with an average blood glucose of 660 mg/dL and an average HbA1cof 8.7%. The exact mechanism PD-1 inhibitor therapy-induced T1DM is unknown. Blood glucose monitoring is recommended for all patients receiving anti-PD-1 therapy. Further research is needed to delineate the frequency of this adverse effect, as well as to evaluate potential risk factors and ideal management strategies.


2015 ◽  
Vol 180 (3) ◽  
pp. 452-457 ◽  
Author(s):  
R. Fujisawa ◽  
F. Haseda ◽  
C. Tsutsumi ◽  
Y. Hiromine ◽  
S. Noso ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (9) ◽  
pp. e0183887 ◽  
Author(s):  
Hector M. Granados ◽  
Andrew Draghi ◽  
Naomi Tsurutani ◽  
Kyle Wright ◽  
Marina L. Fernandez ◽  
...  

2006 ◽  
Vol 1079 (1) ◽  
pp. 285-288 ◽  
Author(s):  
Y. HIROMINE ◽  
H. IKEGAMI ◽  
T. FUJISAWA ◽  
Y. KAWABATA ◽  
S. NOSO ◽  
...  

2016 ◽  
Vol 7 (6) ◽  
pp. 915-918 ◽  
Author(s):  
Masahide Okamoto ◽  
Mitsuhiro Okamoto ◽  
Koro Gotoh ◽  
Takayuki Masaki ◽  
Yoshinori Ozeki ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
Ken Yajima ◽  
Yushi Akise

Immune checkpoint inhibitors, such as anti-programmed cell death-1 (anti-PD-1), have been widely used in the treatment of malignancies. However, these drugs can cause immune-related adverse events resembling autoimmune diseases. There are some reports of Graves’ disease (GD) induced by anti-cytotoxic T-lymphocyte-associated antigen 4 antibodies, but reports which discussed GD induced by anti-PD-1 antibodies are very rare. We report the case of a 61-year-old man with bladder cancer who presented with severe diarrhea, fatigue, palpitation, body weight loss, and hyperthyroidism after the fifth treatment with the anti-PD-1 monoclonal antibody pembrolizumab. His thyroid function prior to pembrolizumab administration had been subclinical hyperthyroidism, despite a negative thyroid-stimulating hormone receptor antibody (TRAb) level. On admission, pembrolizumab administration was discontinued. Graves’ disease was diagnosed based on a positive TRAb test result and the ultrasonographic finding of increased blood flow in the superior thyroid artery. Based on colonoscopy findings, the cause of diarrhea was diagnosed as active colitis. His diarrhea was improved with prednisolone, and thyroid function was treated with potassium iodide and thiamazole. This case report of GD with positive TRAb induced by the anti-PD-1 antibody pembrolizumab may contribute to the understanding of the mechanism underlying the association between GD and autoimmune activation via PD-1.


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