The spectrum of drug-induced liver injury varies from acute hepatitis to chronic hepatitis to acute liver failure. Toxins and medications can cause liver injury through a variety of mechanisms, including direct cell damage, disruption of cell metabolism, and causing structural changes. Some drugs such as paracetamol exhibit predictable dose-dependent liver damage while others such as isoniazid cause idiosyncratic and unpredictable reactions that vary by person. There are wide variations in the mechanisms of liver injury and latency period from exposure to development of clinical illness.Many types of drugs can cause liver injury, including the analgesic paracetamol; antibiotics such as isoniazid, nitrofurantoin, amoxicillin-clavulanate, erythromycin, and trimethoprim-sulfamethoxazole; anticonvulsants such as valproate and phenytoin; cholesterol-lowering statins; steroids such as oral contraceptives and anabolic steroids; and highly active anti-retroviral therapy used in the treatment of HIV/AIDS. Of these, amoxicillin-clavulanate is the most common cause of drug-induced liver injury, and paracetamol toxicity  the most common cause of acute liver failure in the United States and Europe.Herbal remedies and dietary supplements are another important cause of hepatitis; these are the most common causes of drug-induced hepatitis in Korea. The United-States-based Drug Induced Liver Injury Network linked more than 16% of cases of hepatotoxicity to herbal and dietary supplements. In the United States, herbal and dietary supplements – unlike pharmaceutical drugs – are unregulated by the Food and Drug Administration.
Studies of the effectiveness of various drugs for treatment of children with F. buski have shown tetrachloroethylene as capable of reducing faecal egg counts by up to 99%. Other anthelmintics that can be used include thiabendazole, mebendazole, levamisole and pyrantel pamoate. Oxyclozanide, hexachlorophene and nitroxynil are also highly effective. Epidemiology
F. buski is endemic in Asia including China, Taiwan, Southeast Asia, Indonesia, Malaysia, and India. It has an up to 60% prevalence in worst-affected communities in southern and eastern India and mainland China and has an estimated 10 million human infections. Infections occur most often in school-aged children or in impoverished areas with a lack of proper sanitation systems.A study from 1950s found that F. buski was endemic in central Thailand, affecting about 2,936 people due to infected aquatic plants called water caltrops and the snail hosts which were associated with them. The infection, or the eggs which hatch in the aquatic environment, were correlated with the water pollution in different districts of Thailand such as Ayuthaya Province. The high incidence of infection was prevalent in females and children ages 10–14 years of age. References
Further reading
Graczyk TK, Gilman RH, Fried B (2001). "Fasciolopsiasis: is it a controllable food-borne disease?". Parasitol. Res. 87 (1): 80–3. doi:10.1007/s004360000299. PMID 11199855. S2CID 19075125. Mas-Coma S, Bargues MD, Valero MA (2005). "Fascioliasis and other plant-borne trematode zoonoses". Int. J. Parasitol. 35 (11–12): 1255–78. doi:10.1016/j.ijpara.2005.07.010. PMID 16150452.
http://www.ijmm.org/text.asp?2017/35/4/551/224440
Fasciolopsiasis in children: Clinical, Sociodemographic Profile and outcome. Indian Journal of Medical Microbiology2017 vol 35, issue 4 page 551-554DOI:10.4103/ijmm.IJMM_17_7


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