The patients clinical course is shown inFigure 1, and the ADL and QMG scores following eculizumab treatment are presented inFigure 2. == Figure 1. binds to programmed cell death receptor 1 (PD-1), has been reported to induce myasthenia gravis (MG).3Traditional therapies for pembrolizumab-induced MG include glucocorticoids, intravenous immunoglobulin (IVIg), and plasma exchange. However, the clinical outcomes of these therapies remain unsatisfactory. BAY-8002 Here, we present a case of pembrolizumab-induced impending crisis in anti-acetylcholine receptor (AChR) antibody-positive MG. Initiating eculizumab treatment resulted in a rapid response and alleviation of clinical symptoms, with significant improvement in respiratory muscle function. This approach avoided the need for alternative treatments, potentially involving multiple rounds of medication adjustments. Therefore, using eculizumab as rescue therapy provides a viable option for treating pembrolizumab-induced MG due to its rapid therapeutic effects. == Case description == A 75-year-old male was admitted to our hospital on April 30, 2024, due to a 1-week history of ptosis and generalized weakness following the first infusion of pembrolizumab, with symptom worsening over the previous 2 days. One week prior to admission, the patient developed weakness in all limbs and increased fatigue after physical activity. The patient required assistance while walking, was unable to lift both arms, and experienced neck weakness, bilateral ptosis, double vision, and tachypnea following physical activity. He also occasionally choked while drinking water, although he was able to swallow. The patient sought medical attention at a neurology outpatient clinic, where a diagnosis of MG was strongly considered. An MG antibody test was performed using an enzyme-linked immunosorbent assay (ELISA), and treatment with pyridostigmine (30 mg bid) was initiated, which alleviated the patients weakness. Two days prior to admission, his symptoms worsened: he became unable to walk, experienced pronounced tachypnea and dyspnea when lying down, could not sleep in the supine position, and developed orthopnea, which led to his hospitalization. On April 10, 2024, the patient received the first course of pembrolizumab for cholangiocarcinoma, along with capecitabine, an antineoplastic agent. He had a history of hepatitis B infection and cirrhosis for more than 10 years, treated with entecavir. In 2015, he underwent a hepatectomy for liver cancer and made a satisfactory recovery. During the physical examination, the patient was alert and spoke fluently but exhibited orthopnea and pronounced tachypnea. Bilateral ptosis was noted, along with an inability to adduct the right eye, diplopia, and weakness in neck extension. The Medical Research Council scale revealed BAY-8002 1/5 strength in neck flexors/extensors and 2/5 strength in the deltoids, biceps, triceps, quadriceps, and iliopsoas. The patient also tested positive for eyelid easy fatigability. The repetitive nerve stimulation test yielded a positive result. Blood tests showed the following results: lactate, 2.80 mmol/L (elevated); procalcitonin, 0.095 ng/mL (elevated); interleukin-6, 30.23 pg/mL (elevated); quantitative C-reactive protein, 14.55 mg/L (elevated); creatine kinase (CK), 400 U/L (elevated); CK-MB, 2.73 g/L (elevated); lactate dehydrogenase, 289 U/L (elevated); alanine aminotransferase, 55.7 U/L (elevated). Creatinine, routine blood tests, coagulation parameters, and pro-BNP were normal. Electrocardiography revealed sinus tachycardia, and echocardiography was normal. Chest-computed tomography showed reactive inflammation with atelectasis in the lower lobe of the right lung and a small amount of pleural effusion on the right side. Rabbit Polyclonal to FSHR Arterial blood gas (ABG) analysis performed at 18:40 showed a pH of 7.406, partial pressure of CO2(pCO2) of 43 mmHg, and partial pressure BAY-8002 of oxygen (pO2) of 87.2 mmHg. Scores on the Activities of Daily Living (ADL) and Quantitative Myasthenia Gravis (QMG) scales were 12 and 20 points, respectively. A positive serum AChR antibody test result of 35.35 nmol/L (<0.45 nmol/L, ELISA) was obtained. The patient tested negative for anti-MuSK, anti-Lrp4, anti-titin, and serum onconeural antibodies. Based on these findings, the diagnosis of pembrolizumab-induced AChR antibody-positive MGFA Class IVB MG was confirmed. Pyridostigmine (60 mg q6h), prednisone (20 mg), medium-flow oxygen therapy (4 L/min), and ceftriaxone for anti-infective treatment were immediately administered. The patient was only able to maintain orthopnea on exertion and exhibited gradual worsening of tachypnea. Oxygen saturation at the fingertip ranged from 90% to 95% under high-flow oxygen therapy. The patient had previously experienced severe gastrointestinal reactions while taking capecitabine. After increasing the oral dose of pyridostigmine, side.