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Leflunomide, a disease-modifying antirheumatic drug, is effective for rheumatoid arthritis as monotherapy or combination therapy with methotrexate. The most common adverse effects are diarrhea, dyspepsia, nausea, abdominal pain, oral ulcer, hepatotoxicity, skin rash, hypertension, weight loss, and interstitial lung disease. The occurrence of pulmonary cryptococcosis in leflunomide treatment has not been reported in Korea. A 74-year-old woman was admitted to hospital due to asymptomatic pulmonary nodule. She was diagnosed rheumatoid arthritis and treated with leflunomide 5 months ago due to treatment failure with methotrexate, hydroxychloroquine, and sulfasalazine. Chest radiograph and computed tomography showed solitary pulmonary nodule in her right lower lung. Pulmonary cryptococcosis was confirmed by needle biopsy of lung stained with Gomori methenamine silver and mucicarmine. The lesion was improved after antifungal therapy for 3 months. [ABSTRACT FROM AUTHOR]

Background: Aflatoxin B1 (AFB1) is a toxic metabolite generated by Aspergillus species and is commonly detected during the processing and storage of food; it is considered a group I carcinogen. The hepatotoxic effects, diseases, and mechanisms induced by AFB1 owing to chronic or acute exposure are well documented; however, there is a lack of research on its effects on the intestine, which is a crucial organ in the digestive process. Dogs are often susceptible to chronic AFB1 exposure owing to lack of variation in their diet, unlike humans, thereby rendering them prone to its effects. Therefore, we investigated the effects of AFB1 on canine small intestinal epithelial primary cells (CSIc). Methods: We treated CSIc with various concentrations of AFB1 (0, 1.25, 2.5, 5, 10, 20, 40, and 80 μM) for 24 h and analyzed cell viability and transepithelial-transendothelial electrical resistance (TEER) value. Additionally, we analyzed the mRNA expression of tight junction-related genes (OCLN, CLDN3, TJP1, and MUC2), antioxidant-related genes (CAT and GPX1), and apoptosis-related genes (BCL2, Bax, and TP53). Results: We found a significant decrease in CSIc viability and TEER values after treatment with AFB1 at concentrations of 20 μM or higher. Quantitative polymerase chain reaction analysis indiCATed a downregulation of OCLN, CLDN3, and TJP1 in CSIc treated with 20 μM or higher concentrations of AFB1. Additionally, AFB1 treatment downregulated CAT, GPX1, and BCL2. Conclusions: Acute exposure of CSIc to AFB1 induces toxicity, and exposure to AFB1 above a certain threshold compromises the barrier integrity of CSIc.