ECE2022 Eposter Presentations Thyroid (219 abstracts)
Immune checkpoint inhibitors induced myxedema coma
Hatice Sebile Dökmetaş 1 , Meriç Dökmetaş 2 , Ayberk Bayramgil 2 , Kü bra Karaipek 2 , Güneş Dorukhan Çavuşoğlu 2 , Cansu Temiz 2 , Cem İdrisoğlu 2 , Fatih Kılıçlı 1 & Ahmet Bilici 3
1Medipol Mega University Hospital, Endocrinology, Istanbul, Turkey; 2Medipol Mega University Hospital, Internal Medicine, Istanbul, Turkey; 3Medipol Mega University Hospital, Oncology, Istanbul, Turkey
Introduction: Myxedema coma is very rare and its mortality is quite high. It is even rarer to occur due to an immune checkpoint inhibitor.
Case: A 69-year-old patient presented with complaints of dyspnea, fatigue, edema, and hypotension. He had diabetes mellitus, hypertension, and metastatic lung cancer diagnosis. Three weeks ago, he had taken the 10th cycle of atezolizumab for lung cancer, which he had been taking for 7 months. The patient’s body temperature was 35.80 °C, heart rate was 69/min, and arterial blood pressure was 100/50 mmHg. There was sleepiness, apathetic appearance, enlarged tongue, non-pitting edema, abdominal distension, and decreased bowel sounds. In the blood tests of the patient, serum glucose 100 mg/dl (70-100), sodium 115 mmol/l (136-145), TSH 218 µIU/ml (0,2-4,2), free T4 <0,03 ng/dl (0,9-1,7), and anti-thyroglobulin was 483 IU/ml (0-115). The thyroid gland was small and the parenchyma was heterogeneous in the ultrasonography. Blood gas showed hypoxia and hypercapnia. The patient was diagnosed with myxedema coma due to the PDL-1 inhibitor-atezolizumab, which he had taken. Treatment of myxedema coma, mainly intravenous levothyroxine and hydrocortisone, was initiated. After serum-free T4 level returned to the normal range with iv levothyroxine, his treatment with oral 150 mg/d levothyroxine was continued.
Conclusion: As a result of the increasing use of PD-1, PDL-1, and CTLA-4 inhibitors in recent years, also hypothyroidism is the most common endocrine side effect, but myxedema coma is very rare. When all the literature is examined, it is seen rarely that in patients who develop myxedema coma due to immune checkpoint inhibitor. It develops due to PD-1 inhibitors nivolumab and pembrolizumab and CTLA-4 inhibitor ipilimumab. In our case, myxedema coma developed due to atezolizumab, a PDL-1 inhibitor. It should be kept in mind that hypothyroidism and also rarely hypothyroid coma may develop in patients using these drugs.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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