PMC9705572_01
Eyelid ptosis and radiographical presentations of immune-related myocarditis. (A) Both eyelid ptosis occurred at the time of immune-related adverse events (irAEs) onset and improved gradually after the steroid treatment and intravenous immunoglobulin (IVIG). (B) The electrocardiogram showed ectopic heart rhythm and atrial arrhythmia before (upper) and after (lower) the steroid treatment. (C) Temporary right pleural infusion before (upper) and after (lower) the steroid treatment by CT scan. (D) In the third month after the onset of irAEs, the patient received a supplementary cardiac magnetic resonance (MR) examination revealing no edema and hyperemia (left and central), and quantitative myocardial T1 mapping was normal (right). (E) Delayed myocardial enhancement showed patchy enhancement that may be old myocardial injuries resulting from immune-related cardiac toxicity (arrow).
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F1
In May 2021, she began to suffer from limited movement, weakness, and soreness in the bilateral lower extremities that was accompanied with both eyelid ptosis, red to amber-colored transparent urine, and mild dyspnea (Figure 1A). The electrocardiogram showed ectopic heart rhythm and atrial arrhythmia (Figure 1B). She had a right pleural infusion (Figure 1C). A computed tomography (CT) scan showed a temporary right pleural effusion and a slight elevation of BNP (Figures 1C, 2B). Because the patient's performance status improves significantly, 3 months after the onset of immune-related irAEs, she received a supplementary cardiac MR examination revealing no edema and hyperemia, and quantitative myocardial T1 mapping was normal (Figure 1D). Delayed myocardial enhancement showed patchy enhancement that may be old myocardial injuries resulting from immune-related cardiac toxicity (Figure 1E). CT scan showed her right pleural effusion improved completely (Figure 1C).
Illustration of main laboratory markers and steroid treatment following the onset of irAEs. (A) Dynamics of cardiac markers [creatine kinase (CK), creatine kinase isoenzyme (CK-MB), cardiac troponin I (cTnI), and myoglobin (MYO)]. (B) Dynamics of other biochemical markers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and brain natriuretic peptide (BNP)].
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F2
Laboratory examinations showed that creatine kinase (CK) was increased to 1,658 U/L (normal range <140 U/L), creatine kinase isoenzyme (CK-MB) to 124.49 U/L (normal range <25 U/L), cardiac troponin I (cTnI) to 2.35 ng/mL (normal range <0.034 ng/mL), and myoglobin (MYO) to 965.4 ng/mL (normal range <61.5 ng/mL) (Figure 2A). She also had an elevated alanine aminotransferase (ALT) level of 309.1 U/L (normal range <40 U/L), aspartate aminotransferase (AST) level of 154.9 U/L (normal range <35 U/L), and lactate dehydrogenase (LDH) level of 1,616 U/L (normal range <214 U/L), but her brain natriuretic peptide (BNP) was normal (Figure 2B). A computed tomography (CT) scan showed a temporary right pleural effusion and a slight elevation of BNP (Figures 1C, 2B).
Patient timeline chart along with key dates or durations for clinical manifestations, investigations, and treatments with steroids and immunosuppressive agents.
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F3
She was continuedly administrated with oral prednisolone at 60 mg/d for 4 weeks with a slow tapering for an additional 4 weeks (Figure 3).
Clinical diagnosis of immune checkpoint inhibitor (ICI)-related esophageal hiatal hernia. At the sixth (A) and eighth month (B) after the onset of immune-related irAEs, a computed tomography (CT) scan for the first time showed abdominal viscera protruding into the left hemithorax (arrow). Upper gastroenterography and endoscopy showed no esophagitis and inflammation of the gastric body and antrum (C), but a clinically confirmed diagnosis of sliding hiatal hernia of the esophagus (type I) was made (arrow) (D).
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F4
CT scan for the first time showed abdominal viscera protruding into the left hemithorax (Figures 4A,B), and an esophageal hiatal hernia was suspected. Further upper gastroenterography and endoscopy showed no esophagitis and inflammation of the gastric body and antrum (Figure 4C), but a clinically confirmed diagnosis of sliding hiatal hernia of the esophagus (type I) was made (Figure 4D).