Louisiana Research Day Program Book 2025

Case Studies: Section 1

Case Studies: Section 1

Whitney Main Allen, BSc 1 ; Pamraj Sharma, MD 2 ; Mark Megaly, MD 3 1 VCOM-Louisiana; 2 Saint Francis Medical Center Monroe, LA; Dr. Mark Megaly, MD, Internal Medicine, Saint Francis Medical Center Monroe, LA 96 A RARE CASE OF PD-L1 CHECKPOINT INHIBITOR-INDUCED MYOSITIS, MYOCARDITIS, MYASTHENIA GRAVIS (M TRIAD)

Mary Youssief, MS 2 ; Nisheem Pokharel, MD 1 ; Dipesh Upreti, MD 3 , Jeremy Luke Rawson, MD 4 , Matthew Colton Raley, MD 5 1 St. Francis Medical Center; 2 VCOM-Louisiana; 3 St. Francis Medical Center; 4 St. Francis Medical Center; 5 St. Francis Medical Center 97 A RARE CASE OF GEMCITABINE-INDUCED INTERSTITIAL LUNG DISEASE

Background: Checkpoint inhibitors, a class of immunotherapeutic agents, have transformed the landscape of oncology by targeting immune checkpoints, which are regulatory pathways in immune cells. By inhibiting proteins such as PD-1, PD-L1, and CTLA-4, these inhibitors enhance the immune response against cancer cells. However, their efficacy is accompanied by a range of immune-related adverse events, including autoimmune reactions such as colitis, hepatitis, and endocrinopathies, which can vary in severity from mild to potentially life threatening. We present a case of drug-induced immune-mediated myasthenia gravis evidenced by bilateral ptosis, progressive dyspnea, and muscle weakness in a 76-year-old man with signs of overlapping myocarditis. The patient was being treated for Cholangiocarcinoma with the Programmed Cell death ligand 1 (PD-L1) checkpoint inhibitor Durvalumab which resulted in autoimmune-mediated myasthenia gravis. This unique case presents with concurrent cardiac involvement with elevated Troponin levels progressing to arrhythmias with the presence of abnormal electrocardiogram changes in the absence of structural abnormalities identified on testing.

His case ultimately progressed to respiratory failure and death within weeks of onset. Initially, Intravenous immunoglobulin infusion was the mainstay of treatment with some improvement in symptoms briefly noted towards the end of the treatment regimen, but alone was not sufficient to provide full resolution of respiratory weakness or other bulbar signs of the disease. Due to the refractive nature of this immune-mediated disease, the patient received a subsequent dose of intravenous immunoglobulin with prednisone and required plasma exchange at an outside facility. In this report, we present a unique case of a drug-induced triad of myocarditis, myositis, and myasthenia gravis, secondary to PD-L1 inhibitor treatment in a cancer patient where we emphasize the clinical picture at the onset, methods of diagnosis, and interventions.

Introduction: Gemcitabine is an antimetabolite chemotherapeutic agent that is an integral part of regimen as monotherapy and adjuvant therapy in the treatment of a variety of solid malignancies and metastases including breast and pancreatic cancer. In addition to myelosuppression and gastrointestinal toxicity, it can cause lung toxicity that generally presents as mild dyspnea but can rarely result in serious complications ranging from bronchospasm to pneumonitis and pulmonary fibrosis and even respiratory failure. Here we present a case of a patient with Gemcitabine-induced pneumonitis. Case Description: A 72-year-old African American female with a history of metastatic breast cancer, currently undergoing chemotherapy with Gemcitabine (two cycles so far), presented with worsening shortness of breath and bilateral lower extremity swelling. Except for mild tachypnea, the remainder of her vitals were stable. She had crackles on lung auscultation and bilateral lower extremities pitting edema. Her initial chest x-ray indicated moderate bilateral pulmonary infiltrates and pleural effusions. CT pulmonary angiogram revealed subacute to chronic pulmonary

embolism, ground glass opacities suggesting pneumonitis, and small nodules indicating metastatic disease. She initially showed minimal improvement in respiratory symptoms with BIPAP and Lasix. Her extensive infectious workup was unremarkable for pneumonia including negative blood and sputum cultures that prompted suspicion on recently started drug as the possible underlying cause. In the background of initiation of Gemcitabine along with imaging showing pneumonitis, Gemcitabine was discontinued and she was started on Solumedrol with the possibility of Gemcitabine induced pneumonitis. Her condition significantly improved, that eventually led to successful weaning off her oxygen requirement and discharge from the facility. Furthermore, outpatient follow-up revealed restrictive lung disease patterns on pulmonary function test, that further supported the suspected temporality of Gemcitabine. Discussion: Upon review of literature, multiple underlying mechanisms were proposed for Gemcitabine-related interstitial lung injury. Most cases described rapid improvement in lung function after discontinuation of the drug

and minimal supportive care. A high degree of clinical suspicion is required for early recognition and prompt treatment of gemcitabine-induced lung toxicity. Physicians should use clinical symptoms, radiographic findings and rule out other potential etiologies to prevent further morbidity and mortality.

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111 2025 Research Recognition Day