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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-.
Last Update:June 16, 2025.
Turmeric is a spice and popular botanical product derived from the roots of the plant Curcuma longa found mostly in India and Southern Asia. Turmeric has an intense yellow color and distinct taste and is used as a dye as well as a spice in the preparation of curry. Turmeric and its purified extract curcumin are also used medically for their purported antiinflammatory and antioxidant effects to treat a wide variety of conditions and for general health and wellness. Turmeric and curcumin have been associated with a low rate of transient serum enzyme elevations during therapy and, while having a long history of safety, some turmeric products have recently been implicated in several dozen instances of clinically apparent acute liver injury.
Turmeric (tur mer' ik) is a widely used herbal product derived from the roots of Curcuma longa, a perennial plant belonging to the ginger family (Zingiberaceae) that is native to India but grown throughout Southern Asia and in Central America. Extracts of the rhizomes of turmeric contain volatile oils and curcuminoids (such as curcumin, demethoxycurcumin and others) which are believed to be the active antiinflammatory components of the herb and are often collectively referred to as curcumin. Curcumin comprises between 1% and 6% by dry weight of whole turmeric extracts, other components being starch, fats, proteins, fiber, vitamins, minerals, and water. The antiinflammatory effects of turmeric and curcumin are thought to be mediated by inhibition of leukotriene synthesis. Curcumin has also been reported to have antineoplastic effects, mediated perhaps by inhibition of intracellular kinases. Turmeric has been used in traditional Indian (Ayurvedic) medicine to treat many conditions including indigestion, upper respiratory infections and liver diseases. Turmeric and curcumin are under active evaluation as antiinflammatory and antineoplastic agents, for treatment of diabetes and hyperlipidemia and as therapy of liver diseases including nonalcoholic steatohepatitis (NASH). The scientific bases for the purported effects of turmeric are not well established and rigorous proof of its efficacy in any medical condition is lacking. Commercial preparations of turmeric and curcumin vary widely in curcuminoid content. The recommended daily dose varies widely (100 to >1,000 mg daily), depending on the preparation used (curcuminoids vs turmeric extract), formulation (tablets, liquid, root extract, tea) and indications. Side effects are uncommon and mild but may include dermatitis and gastrointestinal upset.
Both turmeric and curcumin were considered to be generally safe and for many years had not been linked to instances of liver injury in any consistent way. Studies of its use in various diseases showed low rates of transient and asymptomatic serum enzyme elevations during therapy, but without instances of clinically apparent acute liver injury. Indeed, turmeric was evaluated as a potential therapy of acute and chronic liver injury, and although its efficacy and safety were not clearly shown, therapy with turmeric and curcumin did not seem to worsen the preexisting liver conditions. Recently, isolated case reports and small case series of liver injury arising during use of turmeric dietary supplements have been published. Initially, these episodes were attributed to other exposures that might have accounted for the injury or possible contaminants in the commercial turmeric products. One reason given for the safety and lack of hepatotoxicity of curcumin was that it is poorly absorbed by the oral route, and it was unclear whether there was adequate systemic exposure to achieve any of the purported beneficial or adverse effects of turmeric or curcumin.
Importantly, means of increasing the bioavailability of curcumin were developed using piperine (black pepper) or lipid nanoparticle delivery methods to increase absorption. These high bioavailability forms of purified curcumin were subsequently linked to several cases of liver injury and mentioned as a possible cause of outbreaks of acute hepatitis with jaundice in Italy. The clinical features of the liver injury attributed to high bioavailable forms of curcumin have recently become better defined. The latency to onset of liver injury has varied from a few weeks to as long as eight months but was typically 1 to 4 months. The onset was insidious with fatigue, nausea and poor appetite followed by dark urine and jaundice. Rash and fever were absent or mild. Laboratory tests at onset typically showed marked elevations in serum aminotransferase levels (often above 1000 U/L) with only mild increases in alkaline phosphatase.Jaundice occurred, particularly if the agent was continued. While signs of hypersensitivity were not prominent, many patients developed autoantibodies, and the clinical syndrome and histological features sometimes resembled autoimmune hepatitis. Prednisone has been used to treat severe cases of turmeric hepatotoxicity but is probably not needed as recovery is rapid once the herbal product is discontinued. While reports of acute liver failure has been attributed to turmeric, most cases resolved completely without evidence of chronic injury or bile duct loss. The hepatocellular pattern of injury and frequency of jaundice suggest that fatal instances might occur at a rate of 10% of jaundiced cases, particularly if the product is not discontinued promptly.
Turmeric appears to have become the most common cause of clinically apparent, herbal-related liver injury in the United States. While most cases are attributed to highly bioavailable forms of curcumin, cases also have been described with use of unadulterated ground turmeric powder and even with turmeric herbal teas. The incidence of clinically apparent liver injury from turmeric is not known but is probably very rare, in the range of 1:10,000 to 1:100,000 persons exposed.
Likelihood score: A (recently established as a well-documented cause of clinically apparent liver injury).
The acute hepatotoxicity caused by turmeric appears to be due to an idiosyncratic injury, perhaps immunologically mediated. Recent reports have shown a close association of turmeric induced liver injury with the HLA allele B*35:01, which was found in over 70% of cases compared to 10% to 15% of controls. This association suggests that the injury is linked to the immune system and perhaps the interaction of curcumin with the HLA molecule that leads to T cell recognition of a self-antigen on liver cells or to curcumin adducts present on liver cell membranes. The HLA-B* 35:01 allele is also linked to liver injury due to green tea (Camellia sinensis), Garcinia cambogia, and fo-ti (Polygonum multiflorum). These 4 herbs all have bioactive constituents that are polyphenols.
Most cases of acute hepatic injury from turmeric resolve within 1 to 3 months of stopping the medication. In some instances, however, the injury is severe and unremitting, leading to acute liver failure and either death or need for liver transplantation. A severe outcome is more likely if turmeric is continued after the appearance of symptoms and signs of liver injury. There appears to be no cross sensitivity to hepatic injury between turmeric and other herbal products. However, reexposure to turmeric should be avoided as recurrence and more severe liver injury can occur with rechallenge.
Drug Class:Herbal and Dietary Supplements
A 57 year old woman with recurrent urinary tract infections, migraine headaches, and osteoarthritis developed fatigue, nausea, abdominal pain, and anorexia, followed by itching, dark urine, and jaundice. Because of a recurrence of cystitis, she had received a 7-day course of nitrofurantoin 4 months previously and a 7-day course of cephalexin a few weeks previously. Because of persistence of symptoms, she started an over-the-counter preparation of turmeric (Nature’s Way Turmeric, 500 mg once daily) 2 to 3 weeks before onset of symptoms. She had no history of liver disease, did not drink alcohol, and had no risk factors for viral hepatitis. Her other medications included rizatriptan, salbutamol, vitamin C and D, and a multivitamin. On presentation, her serum bilirubin was 9.1 mg/dL,ALT 1425 U/L,AST 1374 U/L, and alkaline phosphatase 250 U/L and she was admitted to a hospital for evaluation. The INR was 1.3 and albumin 3.7 g/dL. Tests for hepatitis A, B, and C were negative. The ANA was positive (1:640), but SMA and AMA were negative and IgG levels were normal (1170 mg/dL). Abdominal ultrasound showed a right renal stone without hydronephrosis and normal appearing liver without evidence of biliary obstruction or gallstones. A liver biopsy showed acute inflammation and necrosis with eosinophils; plasma cells were not prominent and there was no fibrosis. Turmeric had been stopped and her liver tests improved rapidly without specific therapy (see Table). Serum bilirubin levels fell into the normal range within 6 weeks and aminotransferase levels within 3 months of stopping turmeric. When seen in follow up a year after onset, she was asymptomatic, and all liver tests were normal.
| Medication: | Turmeric (500 mg once daily) |
|---|---|
| Pattern: | Mixed (R=13.7) |
| Severity: | 3+ (jaundice, hospitalization) |
| Latency: | 3 weeks |
| Recovery: | Complete within 2 months |
| Other medications: | Rizatriptan, salbutamol, vitamins |
| Time After Starting | Time After Stopping | ALT (U/L) | Alk P (U/L) | Bilirubin (mg/dL) | Other |
|---|---|---|---|---|---|
| 0 | Started Turmeric (500 mg daily) | ||||
| 3 weeks | -1 week | Developed symptoms of fatigue, nausea | |||
| 4 weeks | 0 | Stopped turmeric | |||
| 5 weeks | 7 days | 1425 | 250 | 9.1 | Admitted |
| 9 days | 1145 | 306 | 11.5 | Liver biopsy | |
| 6 weeks | 14 days | 747 | 268 | 8.1 | Discharged |
| 7 weeks | 21 days | 466 | 292 | 4.8 | |
| 9 weeks | 34 days | 95 | 183 | 2.5 | |
| 48 days | 40 | 170 | 1.4 | ||
| 3 months | 34 | 136 | 1.1 | ||
| 1 year | 18 | 104 | 0.7 | ||
| Upper Limit of Normal | 50 | 125 | 1.2 | ||
A middle aged woman developed acute, icteric hepatitis 2 to 3 weeks after starting turmeric for recurrent urinary tract infections that had not responded to nitrofurantoin or cephalosporins. The liver injury began to improve within 1-2 weeks of stopping the turmeric and without other specific therapy. The turmeric product tested positive for curcumin and was negative for other potentially toxic herbal products as well as black pepper. The patient was homozygous for HLA-B*35:01, an HLA allele closely linked to liver injury from several herbal products including turmeric, green tea, Fo-ti, and garcinia. The clinical features of female sex, hepatocellular liver injury, low levels of autoantibodies, lack of rash and fever, and rapid improvement on stopping the product are typical of turmeric induced liver injury. While she had also been exposed to nitrofurantoin and cephalexin, the latency to onset was not compatible with those two antibiotics and cephalexin is a very rare cause of liver injury which is typically cholestatic.
A 35 year old man with chronic low back pain developed fatigue, low grade fever, nausea, vomiting followed by itching, dark urine, and jaundice having taken a dietary supplement of curcumin for the previous two months (Nature’s Lab: Curcumin C3 1,000 mg with BioPerine [black pepper: 5 mg]). He was found to be jaundiced with a total bilirubin of 12.5 mg/dL,ALT 2014 U/L,AST 796 U/L, and alkaline phosphatase 124 U/L (R value 43). His other medications included ibuprofen, “Move Free Joint Support” (glucosamine, chondroitin sulfate and Boswellia), collagen powder, fish oil, vitamins B and C, and a daily multivitamin, all of which he had taken for 9 months or more. He was admitted for evaluation and management. Tests for hepatitis A, B, and C were negative. The ANA was positive (1:160), but SMA and AMA were negative. An ultrasound was normal. Despite discontinuation of the curcumin and treatment with methylprednisolone for 6 days, he remained jaundiced. A liver biopsy showed marked portal and lobular inflammation with lymphocytes and eosinophils but scant plasma cells. He was discharged and followed as an outpatient on antihistamines and cholestyramine for pruritus. Serum enzymes and bilirubin levels gradually decreased and fell into the normal range two months after initial presentation. When seen in follow up 1 year after onset, he was asymptomatic, and all liver tests were normal.
| Medication: | Curcumin (1,000 mg once daily) with black pepper |
|---|---|
| Pattern: | Hepatocellular (R=43) |
| Severity: | 3+ (jaundice, hospitalization) |
| Latency: | 2 months |
| Recovery: | Complete within 2 months |
| Other medications: | Chondroitin, glucosamine, Boswellia, fish oil, collagen, vitamins |
| Time After Starting | Time After Stopping | ALT (U/L) | Alk P (U/L) | Bilirubin (mg/dL) | Other |
|---|---|---|---|---|---|
| 0 | Started curcumin (1000 mg daily with black pepper) | ||||
| 6 weeks | Developed symptoms of fatigue, nausea | ||||
| 2 months | 0 | 2014 | 125 | 12.5 | Admitted, curcumin stopped |
| 1 day | 1535 | 114 | 11.8 | Methylprednisolone, 6 days | |
| 6 weeks | 2 days | 1106 | 74 | 8.5 | |
| 7 weeks | 12 days | 780 | 81 | 14.0 | |
| 9 weeks | 14 days | 730 | 92 | 14.0 | Discharged |
| 20 days | 486 | 75 | 9.7 | ||
| 4 weeks | 795 | 69 | 5.2 | ||
| 5 weeks | 313 | 65 | 2.6 | ||
| 7 weeks | 52 | 51 | 1.8 | ||
| 2 months | 38 | 60 | 1.7 | ||
| 1 year | 16 | 54 | 1.3 | Final follow up | |
| Upper Limit of Normal | 50 | 125 | 1.2 | ||
A young man started an herbal supplement with high levels of curcumin (1 gram) and black pepper (5 mg) and developed a moderately severe acute hepatitis with jaundice two months later. He had some features of autoimmunity and was treated with methylprednisolone but had little or no response and the corticosteroid was stopped. Eventually he began to improve on his own, symptoms resolved, and liver tests fell into the normal range by 2 months after stopping the supplement. The curcumin product was tested chemically and found to contain both curcumin and black pepper as labelled; no other herbal product or toxin was identified. The patient had some features of autoimmunity (ANA positivity) but the liver biopsy was more compatible with drug induced liver injury, and he didn’t improve during a short trial of corticosteroids. Subsequent testing revealed that he was heterozygous for HLA- B*35:01, an allele strongly associated with hepatic injury caused by herbals that are rich in polyphenols (such as turmeric, green tea, polygonum multiflora, and garcinia).
A 62 year old woman developed fatigue and nausea followed by dark urine and jaundice having taken a turmeric root extract (Rite Aid: Turmeric, 500 mg) once daily for wellbeing and arthritis for the previous 14 months. She had no history of liver disease, excessive alcohol intake, or risk factors for viral hepatitis. Her medical conditions included osteoarthritis, season allergies, menopausal symptoms, and uterine fibroids. Her medications included estrogens, pseudoephedrine, diphenhydramine, salbutamol, tramadol, magnesium, fish oil, ginger, glucosamine, vitamins C and D, and a multivitamin, all of which she had taken for more than a year. She stopped the turmeric and 3 days later was seen and found to have abnormal liver tests (bilirubin 2.5 mg/dL,ALT 1230 U/L,AST 1628 U/L, alkaline phosphatase 329 U/L). She was admitted to the hospital briefly. Tests for hepatitis A, B, C and E and for CMV and HSV infection were negative as were routine autoantibody and serum IgG levels. She was discharged and followed as an outpatient, but her condition worsened with bilirubin rising to 13.5 mg/dL and INR to 2.0. She was readmitted. Imaging of the liver showed evidence of diffuse hepatocellular disease, a nodular liver, and ascites. She was listed for emergency liver transplantation but suffered an acute myocardial infarction and ultimately developed multiorgan failure and died one month after initial presentation. An autopsy showed a shrunken liver, massive hepatic necrosis, a ruptured posterior leaflet of the mitral value, and recent myocardial infarction.
| Medication: | Turmeric 500 mg daily |
|---|---|
| Pattern: | Hepatocellular (R=14) |
| Severity: | 5+ (death within six months of onset from acute liver failure) |
| Latency: | 14 months |
| Recovery: | None |
| Other medications: | Estrogens, pseudoephedrine, diphenhydramine, salbutamol, tramadol, fish oil, magnesium, glucosamine, ginger, vitamins |
| Time After Starting | Time After Stopping | ALT (U/L) | Alk P (U/L) | Bilirubin (mg/dL) | INR | Other |
|---|---|---|---|---|---|---|
| 0 | Started Turmeric (500 mg daily) | |||||
| 14 months | 0 | Curcumin stopped, symptoms of fatigue and jaundice | ||||
| 3 days | 1230 | 329 | 2.5 | Admitted | ||
| 7 days | 1360 | 333 | 6.1 | Methylprednisolone, 6 days | ||
| 10 days | 1277 | 311 | 8.6 | 1.5 | Discharged | |
| 13 days | 1088 | 251 | 13.5 | 2.0 | ||
| 17 days | 898 | 329 | 17.5 | 1.4 | Readmission | |
| 19 days | 704 | 303 | 18.7 | 2.3 | ||
| 15 months | 20 days | 513 | 249 | 16.8 | 2.1 | Acute myocardial infarction |
| 22 days | 530 | 280 | 23.6 | 2.3 | ||
| 26 days | 171 | 160 | 22.8 | 2.5 | Listed for liver transplantation | |
| 33 days | Died of multiorgan failure | |||||
| Upper Limit of Normal | 35 | 135 | 1.2 | |||
A 62 year old woman developed a severe acute hepatitis 14 months after starting turmeric. No other cause for the liver injury was identified. The liver injury did not improve with stopping turmeric and within 3 weeks she demonstrated evidence of acute liver failure. She was listed for liver transplantation but developed an acute myocardial infarction and rapidly developed multiorgan failure and died within 5 weeks of onset. Chemical analysis was done on the herbal product which demonstrated the presence of turmeric without black pepper or other potentially hepatotoxins or herbs. The patient was negative for HLA-B*35:01. The case was judged to be only “probable” liver injury due to turmeric. Against the diagnosis was the long latency (greater than a year), lack of improvement with stopping the herbal product, and absence of HLA-B*35:01.
REPRESENTATIVE TRADE NAMES
Turmeric – Generic
DRUG CLASS
Herbal andDietary Supplements
COMPLETE LABELING
Fact Sheet at National Center for Complementary and Integrative Health
| DRUG | CAS REGISTRY NUMBER | MOLECULAR FORMULA | STRUCTURE |
|---|---|---|---|
| Turmeric | 458-37-7 | C21-H20-O6 |
References updated: 16 June 2025
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