It may manifest as a very high level of ALT and severe disturbance of liver function leading to acute liver failure. Causes include:
Paracetamol, carbon tetrachloride

Hepatitis
In this pattern, hepatocellular necrosis is associated with infiltration of inflammatory cells. There can be three types of drug-induced hepatitis. (A) viral hepatitis is the most common, where histological features are similar to acute viral hepatitis. (B) in focal or non-specific hepatitis, scattered foci of cell necrosis may accompany lymphocytic infiltration. (C) chronic hepatitis is very similar to autoimmune hepatitis clinically, serologically, and histologically. Causes:
(a) Viral hepatitis: Halothane, isoniazid, phenytoin
(b) Focal hepatitis: Aspirin
(c) Chronic hepatitis: Methyldopa, diclofenac

Cholestasis
Liver injury leads to impairment of bile flow and cases are predominated by itching and jaundice. Histology may show inflammation (cholestatic hepatitis) or it can be bland (without any parenchymal inflammation). On rare occasions, it can produce features similar to primary biliary cirrhosis due to progressive destruction of small bile ducts (vanishing duct syndrome). Causes:
(a) Bland: Oral contraceptive pills, anabolic steroid, androgens
(b) Inflammatory: Allopurinol, co-amoxiclav, carbamazepine
(c) Ductal: Chlorpromazine, flucloxacillin

Steatosis
Hepatotoxicity may manifest as triglyceride accumulation, which leads to either small-droplet (microvesicular) or large-droplet (macrovesicular) fatty liver. There is a separate type of steatosis by which phospholipid accumulation leads to a pattern similar to the diseases with inherited phospholipid metabolism defects (e.g., Tay–Sachs disease)

Causes:
(a) Microvesicular: Aspirin (Reyes syndrome), ketoprofen, tetracycline (especially if expired)
(b) Macrovesicular: Acetaminophen, methotrexate
(c) Phospholipidosis: Amiodarone, total parenteral nutrition
(d) Antiviral: nucleoside analogues
(e) Corticosteroid
(f) Hormonal: Tamoxifen

Granuloma
Drug-induced hepatic granulomas are usually associated with granulomas in other tissues and patients typically have features of systemic vasculitis and hypersensitivity.
(1997) Correlation of tumor necrosis factor levels in the serum and cerebrospinal fluid with clinical outcome in Japanese encephalitis patients. J Med Virol 51: 132–136. Kumari P, Yadav P, Verma PR, Kumar, Arya, Kumar S, et al. (2013) A review on wound healing properties of Indian medicinal plants. Ind J Fund Appl Life Sci 3: 220–232. Kumar A, Agarwal K, Maurya AK, Shanker K, Bushra U, et al. (2015) Pharmacological and phytochemical evaluation of Ocimum sanctum root extracts for its anti-inflammatory, analgesic and antipyretic activities. Pharmacogn Mag 11: S217. Ranjana T, Tripathi V (2015) Therapeutic effect of tulsi (Ocimum sanctum Linn) in general and oral health. Ayurlog: National Journal of Research in Ayurveda Science 3: 1–12. Suanarunsawat T, Ayutthaya WDN, Thirawarapan S, Poungshompoo S (2014) Anti-oxidative, anti-hyperglycemic and lipid-lowering effects of aqueous extracts of Ocimum sanctum L. leaves in diabetic rats. Food Nutr Sci 5: 801–811. Talekar, Y. P., Das, B., Paul, T., Talekar, D. Y., Apte 1, K. G., & Parab, P. B. (2012). Evaluation of hepatoprotective Potential of Aqueous and Ethanolic Extract of Ocimum sanctum Linn. In Wistar Rats. Asian Journal of Pharmaceutical and Clinical Research, 5(4), 141–145. Singh V, Kumar R.(2017).Study of Phytochemical Analysis and Antioxidant Activity of Allium sativum of Bundelkhand Region. International Journal of Life Sciences Scientific Research. 3(6):1451-1458. Raaman N.(2006). Phytochemical Techniques. New India Publishing Agency, New Delhi, 19–24. Tiwari P, Kumar B, Kaur M, Kaur G, Kaur H.(2011). Phytochemical screening and Extraction: A Review. Internationale Pharmaceutica Sciencia. 1(1):98-106.