Aim
Evidence is lacking on the best standard method for forced diuresis to prevent cisplatin‐induced nephrotoxicity. We compared the cisplatin‐induced nephrotoxicity prevention effect of furosemide or mannitol in patients with advanced non‐small cell lung cancer.
Methods
Patients with advanced non‐small cell lung cancer suitable to receive cisplatin‐containing regimen were randomly assigned to receive furosemide or mannitol with appropriate hydration. The primary endpoint was the proportion of ≥ grade 1 serum creatinine elevation in the first cycle.
Results
The trial was terminated early with 44 (22 per arm) of the planned 66 patients because of slow accrual. Patients’ characteristics were well balanced with median baseline creatinine clearance of 98.0 and 95.1 mL/min in the furosemide and mannitol arms, respectively. In the first cycle, two (9%) and four (18%) patients developed grade 1 creatinine elevation (P = .66), respectively, despite no ≥ grade 2 toxicity. The median times to develop the worst creatinine score were 10 and 8 days, respectively. For all cycles, median times to recover to grade 0 were 56 and 20 days, respectively. The furosemide arm was characterized by relatively high urine output after cisplatin administration (900 vs 550 mL/h), low frequency of unplanned additional hydration (14% vs 32%), and high incidence of hyponatremia (18% and 5%) compared with the mannitol arm. Both arms showed similar progression‐free survival and overall survival.
Conclusion
The preventive effect of the two forced diuretics on cisplatin‐induced nephrotoxicity was not significantly different. However, the two diuretics have some distinct types of clinical presentations.
Alectinib is a key drug for treating anaplastic lymphoma kinase (ALK)-positive non-small-cell lung cancer (NSCLC). Alectinib-induced hepatotoxicity is less common than that through other ALK inhibitors, such as crizotinib or ceritinib. Herein, we describe a case of ALK-positive adenocarcinoma successfully treated with lorlatinib after developing alectinib-induced hepatotoxicity. A 57-year-old Japanese man received alectinib as first-line therapy for ALK-positive NSCLC. After 79 days, alectinib was discontinued because of hepatotoxicity and later restarted at 150 mg/day, inducing hepatotoxicity again after 64 days. Switching to lorlatinib treatment (continued for >4 months) caused no severe adverse effects. Hence, lorlatinib may be useful for patients experiencing alectinib-induced hepatotoxicity.
Cases of inferior phrenic artery-to-pulmonary artery fistulas and those complicated by massive hemoptysis have been rarely reported. A 38-year-old man presented to our hospital with a chief complaint of coughing. Computed tomography (CT) revealed a nodule in the left lower lobe, and contrast-enhanced CT showed inflow of contrast medium into the nodule. CT angiography detected an aneurysm associated with a left inferior phrenic artery-to-left pulmonary artery fistula. Transcatheter arterial embolization (TAE) was performed to prevent hemoptysis. Hemoptysis did not occur during the 2-year follow-up. We report a rare case of asymptomatic aneurysm associated with a left inferior phrenic artery-to-left pulmonary artery fistula, which was successfully treated using TAE to prevent hemoptysis.
Heerfordt's syndrome is a rare subtype of sarcoidosis and features a combination of facial palsy, parotid swelling, and uveitis, associated with a low-grade fever. Cases with two of three symptoms are called “incomplete Heerfordt's syndrome.” Heerfordt's syndrome involving other cranial nerve symptoms is relatively rare. We herein report a case of incomplete Heerfordt's syndrome presenting with trigeminal nerve palsy and a reversed halo sign, a rare manifestation of pulmonary sarcoidosis. The histological diagnosis following a biopsy of the parotid gland and endobronchial ultrasound-guided trans-bronchial needle aspiration of the mediastinal lymph nodes was sarcoidosis. The symptoms and lung lesions improved after corticosteroid therapy.
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