Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiosyncratic drug-induced liver injury (DILI) is ranked among the top most common etiologies of acute liver failure (ALF). It carries poor transplant-free survival. Pirfenidone is an anti-inflammatory and antifibrotic drug that is commonly used for the treatment of idiopathic pulmonary fibrosis (IPF). Hepatotoxicity due to pirfenidone is rare and generally manifests as a mild rise in serum aminotransferases. In this mini-review, we report an unusual case of idiosyncratic DILI due to pirfenidone presenting as ALF, with emphasis on the definition, classification, diagnostic criteria, histopathology, molecular markers, and treatment options for DILI and related ALF. A 77-year-old man with known Parkinson's disease and IPF presented with jaundice for 7 days and altered mental status for 4 days. His long-term medications included a levodopa/carbidopa combination with a recent addition of pirfenidone over the previous 1 month; there was no monitoring of liver function tests. The evaluation suggested features of acute liver failure with grade III hepatic encephalopathy, acute kidney injury, and metabolic acidosis. The diagnostic workup ruled out viral, toxic, ischemic, and other etiologies for acute liver failure. Based on a Roussel Uclaf Causality Assessment Method score of 7 and possible DILI-ALF, pirfenidone was withdrawn. He was evaluated for liver transplantation but was declined. Despite all supportive measures in intensive care, organ failure progressed and he succumbed to the illness on day 4. Postmortem liver biopsy revealed findings consistent with DILI (final Roussel Uclaf Causality Assessment score, 10). Conclusion: DILI-ALF carries poor prognosis, and liver transplantation should be considered early in the course. Characterization, reporting, monitoring, and labeling of pirfenidone-related hepatotoxicity is vital given its common use in IPF. (Hepatology Communications 2018;2:142-147).
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PMID:Drug idiosyncrasy due to pirfenidone presenting as acute liver failure: Case report and mini-review of the literature. 2940 21

Cadmium (Cd) is a significant ecotoxic heavy metal that adversely affects all biological processes of humans, animals and plants. Exposure to acute and chronic Cd damages many organs in humans and animals (e.g. lung, liver, brain, kidney, and testes). In humans, the Cd concentration at birth is zero, but because the biological half-life is long (about 30 years in humans), the concentration increases with age. The industrial developments of the last century have significantly increased the use of this metal. Especially in developing countries, this consumption is higher. Oxidative stress is the imbalance between antioxidants and oxidants. Cd increases reactive oxygen species (ROS) production and causes oxidative stress. Excess cellular levels of ROS cause damage to proteins, nucleic acids, lipids, membranes and organelles. This damage has been associated with various diseases. These include cancer, hypertension, ischemia/perfusion, cardiovascular diseases, chronic obstructive pulmonary disease, diabetes, insulin resistance, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, asthma, skin diseases, chronic kidney disease, eye diseases, neurodegenerative diseases (amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease, and Huntington disease). Natural antioxidants are popular drugs that are used by the majority of people and have few side effects. Natural antioxidants play an important role in reducing free radicals caused by Cd toxicity. Our goal in this review is to establish the relationship between Cd and oxidative stress and to discuss the role of natural antioxidants in reducing Cd toxicity.
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PMID:The Role of Natural Antioxidants Against Reactive Oxygen Species Produced by Cadmium Toxicity: A Review. 3237 87