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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-.

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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet].

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Khat

Last Update: January 29, 2024.

OVERVIEW

Introduction

Khat is a stimulant derived from the fresh leaves of the evergreen shrub Catha edulis, which is native to parts of East Africa and the Arabian Peninsula. Chewing khat leaves is a well established social habit in areas where the shrub is endemic and causes a mild euphoria. Khat chewing has been implicated in causing rare but serious, clinically apparent acute and chronic liver injury.

Background

Khat (pronounced "kaat") is a product of the leaves of the evergreen shrub Catha edulis that is native to Ethiopia, Kenya, North Yemen and Madagascar. Chewing the leaves releases a stimulant that is absorbed through the oral mucosa and results in mild stimulation, heightened sense of awareness and euphoria. Khat chewing is a common practice and social habit, particularly among men in areas of East Africa and the Arabian Peninsula where the shrub is endemic. Recently, immigrants from those countries have introduced the practice to other areas of the world, including North America, Europe, and Australia. The active ingredient of khat is believed to be phenylalkylamine alkaloids (cathinone, cathine and nor pseudoephedrine), which have sympathomimetic effects that resemble those of the amphetamines. Khat has no current medicinal use and is considered a drug of abuse with potentially serious psychological and neurological adverse effects. Khat is banned in the United States, but is legal and available in Africa, the Middle East, and some countries in Europe including the UK. Common side effects of chewing khat include excitation, confusion, decreased appetite, hyperactivity, hypertonia and hyperthermia. Chronic use has been linked to disruption of personal and family relations, depression, psychiatric problems, hypertension, myocardial infarction and stroke.

Hepatotoxicity

There is little information of whether acute or chronic khat use is associated with serum enzyme elevations or alterations in liver function. However, in recent years several individual case reports and small case series of serious acute and chronic liver injury attributed to khat have been published, largely from the UK and Europe and in immigrants from areas of the world where khat use is frequent. The onset of injury usually occurs after years of khat use and can present acutely with nausea, fatigue, pruritus and jaundice or chronically, with signs and complications of portal hypertension. The pattern of liver enzyme elevations is typically hepatocellular and, in acute cases, the aminotransferase levels can be markedly elevated. Autoantibodies occur in a proportion of cases and the disease often resembles autoimmune hepatitis with chronic inflammation and fibrosis. However, responses to corticosteroid therapy are usually only partial, at least if khat use continued. Immunoallergic features (rash, fever, eosinophilia) are not common. Some patients suffer from multiple bouts of acute injury which leads to fibrosis and cirrhosis, portal hypertension and hepatic failure. Resolution occurs if khat chewing is stopped, but relapses are common, even in some patients who deny relapse in khat use. While most cases have been described from Europe and North America, chronic liver disease and cirrhosis of unknown cause are frequent in areas of the world where khat is commonly used.

Likelihood score: B (highly likely cause of clinically apparent liver injury).

Mechanism of Liver Injury

Khat leaves have multiple components, some of which may be hepatotoxic. In animals, liver injury and fibrosis have been reproduced by chronic khat exposure. Interestingly, liver injury specifically related to khat has not been reported from areas of the world where it is commonly used, despite some studies specially focusing on the frequency of liver injury among chronic khat users. In these countries where Catha edulis is endemic and common, only freshly cut khat leaves are used and they are typically sold the day that they are harvested. Thus, the liver injury associated with khat use that has been reported from North America, Europe and Australia may be related to the storage and shipping of the leaves, either from a contaminant or a breakdown product during storage. There is a superficial resemblance of the liver injury from khat to that of amphetamines, particularly methylenedioxymethamphetamine (MDMA, ecstasy). Contamination with ecstasy might be done to enhance the euphoric effects of khat, especially in long stored leaves that typically have less cathinone due to its metabolism.

Outcome and Management

The liver injury attributed to khat use can be severe and progressive, but resolution has been reported in patients who have stopped use of khat. Because khat use can result in psychological and physical dependence, stopping its regular use may be difficult. Corticosteroids are often used in patients who present with autoimmune features, but they appear to have little effect in khat related liver injury and should not be considered routine therapy. Liver transplantation has been successful in some patients, with end stage liver disease attributed to khat chewing.

Drug Class: Agents of Abuse; Herbal and Dietary Supplements

CASE REPORT

Case 1. Recurrent acute hepatitis attributed to Khat.(1)

A 24 year old man presented with a one week history of jaundice and fatigue and was found to have abnormal liver tests. He was otherwise healthy, denied a history of alcohol or drug use, was taking no medications, and had no risk factors for viral hepatitis. Laboratory tests showed a total bilirubin of 11.2 mg/dL, ALT 2449 U/L, and AST 1388 U/L. Alkaline phosphatase levels were not provided. Importantly, the INR was elevated at 1.6 qualifying the case as being severe. Abdominal ultrasound was normal. A percutaneous liver biopsy showed a cholestatic hepatitis with eosinophils and plasma cells but little interface hepatitis. Tests for viral hepatitis, and other potential viral causes were negative. Over 8 days of hospitalization he improved clinically, and serum enzymes decreased (Table). After discharge he did not return for follow up but presented two months later with a similar acute history and similar laboratory abnormalities. At this point he admitted to use of khat. He was born in Somalia, lived for several years in India, and had immigrated to Canada three years previously. He admitted to chewing khat (a common practice among Somali immigrants) 4 or 5 times monthly in recent years in Canada. His prior use in Somalia was not provided. Again, his symptoms and laboratory abnormalities improved during an 8 day hospitalization but were still abnormal at discharge, the INR being 1.6. Note that the second episode was more severe, with an INR of 1.9 and a higher AST to ALT ratio. He was strongly advised to avoid further use of khat. He again did not return for follow up.

Key Points

Medication:Khat
Pattern:Hepatocellullar (R=unable to calculate)
Severity:4+ (jaundice, hospitalization, INR prolonged)
Latency:Three years of weekly khat use
Recovery:Uncertain in timing and degree
Other medications:None

Laboratory Values

Days After
Stopping		ALT
(U/L)		AST
(U/L)		INRBilirubin
(mg/dL)		Other
1244913881.611.1Admission
3228411691.616.9Liver biopsy
815318861.614.8Discharged
2 monthsDid not return in follow up, and evidently returned to regular khat use
1182714841.916.6Readmitted
3166913731.612.8History of khat use obtained
89146461.66.4Discharged
Again, he did not return in follow up

Comment

The history and presentation of this case were typical of khat hepatotoxicity as seen in Europe and North America. The onset can be sudden despite long term use and no previous symptoms or signs of liver injury. The liver biopsy showed acute hepatitis with scant fibrosis, but the injury was clearly severe and multiple such bouts would likely result in cirrhosis. The lack of mentioning khat use during the first admission and the lack of follow up are also typical of khat hepatotoxicity. It is illegal and addictive. The patient likely lacked medical insurance or resources to obtain regular medical care. The major psychotropic agent in khat is cathinone, an amphetamine-like central nervous system stimulant. Interestingly, the clinical presentation, course, and potential for causing cirrhosis with continued use resemble the liver injury from ecstasy (methylenedioxymethamphetamine: MDMA).

PRODUCT INFORMATION

REPRESENTATIVE STREET NAMES

Khat – Abyssinian Tea, Chat, Gat, Kat, Miraa, Oat, Qat, Somali Tea

DRUG CLASS

Agents of Abuse; Herbal and Dietary Supplements

SUMMARY INFORMATION

Fact Sheet at Drug Enforcement Administration

Information at Drug & Chemical Evaluation Section, Drug Enforcement Administration

CHEMICAL FORMULA AND STRUCTURE

DRUGCAS REGISTRY NO.MOLECULAR FORMULASTRUCTURE
Cathinone 5265-18-9 C9-H11-N-OSID: 135064802

CITED REFERENCE

1.
Waters M, Oxner A, Krajden S, Sultanian R. Acute liver injury associated with khat use in a 24-year-old male. Case Reports Hepatol. 2018;2018:2816907. [PMC free article: PMC6280303] [PubMed: 30584482]

ANNOTATED BIBLIOGRAPHY

References updated: 29 January 2024

Abbreviations: HDS, herbal and dietary supplements.

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    (Expert review of hepatotoxicity published in 1999; discussion of hepatotoxicity of herbal and dietary supplements does not include mention of khat).
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    (Review of hepatotoxicity of herbal and dietary supplements; does not mention or discuss khat).
  • Khat. In, PDR for Herbal Medicines. 4th ed. Montvale, New Jersey: Thomson Healthcare Inc. 2007: pp 497-8.
    (Compilation of short monographs on herbal medications and dietary supplements including khat).
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  • Chaudier B, Oliver M, Coton T, Civatte M, Guisset M, Carré, Debonne JM, Delpy R. [Chronic hepatitis with an acute presentation due to Ecstasy]. Gastroenterol Clin Biol 2002; 26: 103-4. French. [PubMed: 11938056]
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  • Toennes SW, Harder S, Schramm M, Niess C, Kauert GF. Pharmacokinetics of cathinone, cathine and norephedrine after the chewing of khat leaves. Br J Clin Pharmacol 2003; 56: 125-30. [PMC free article: PMC1884326] [PubMed: 12848785]
    (Formal pharmacokinetic study demonstrated effective extraction of cathinone and related alkaloids [>90%] from chewing khat leaves, probable oral absorption, high rapid peak levels and half life of 1.5 hours).
  • Carvalho F. The toxicological potential of khat. J Ethnopharmacol 2003; 87: 1-2. [PubMed: 12787946]
    (Editorial on toxicological profile of khat, its common side effects being withdrawal symptoms, depression, irritability, anorexia, hyperthermia, and insomnia; long term use may be associated with hypertension, cardiovascular events and esophageal cancer).
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    (35 year old East African man living in London developed jaundice and pruritus, having started using khat "recently" on a daily basis [bilirubin 10.6 mg/dL, ALT 2732 U/L, Alk P 231 U/L, ANA negative], ultimately resolving after stopping khat).
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    (Review of the components, chemical structures, pharmacology, and actions of khat).
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    (Among 300 cases of drug induced liver disease in the US collected between 2004 and 2008, 9% were attributed to herbal and dietary supplements, but none to khat).
  • Balint EE, Falkay G, Balint GA. Khat – a controversial plant. Wien Klin Wochenschr 2009; 121 (19-20): 604-14. [PubMed: 19921126]
    (Thorough review of the history and current use of khat, its chemical constituents, pharmacology, biologic effects, and side effects; fibrosis and cirrhosis are listed as adverse effects, but not commented upon).
  • Reuben A, Koch DG, Lee WM; Acute Liver Failure Study Group. Drug-induced acute liver failure: results of a U.S. multicenter, prospective study. Hepatology 2010; 52: 2065-76. [PMC free article: PMC3992250] [PubMed: 20949552]
    (Among 1198 patients with acute liver failure enrolled in a US prospective study between 1998 and 2007, 133 were attributed to drug induced liver injury, of which 12 were attributed to herbal supplements, but none to khat).
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    (Brief description of 6 patients who were immigrants from Africa or the Arabian Peninsula living in the UK with severe liver disease attributed to chewing khat for 6-10 years, 5 requiring liver transplant, most with multiple episodes of acute liver injury [while in the UK], resulting in liver failure [bilirubin 9.6-23.3 mg/dL, ALT 244-2314 U/L, Alk P 193-258 U/L, INR 1.3-3.7]).
  • Peevers CG, Moorghen M, Collins PL, Gordon FH, McCune CA. Liver disease and cirrhosis because of Khat chewing in UK Somali men: a case series. Liver Int 2010; 30: 1242-3. [PubMed: 20408953]
    (Brief description of 7 Somalian men seen over 10-year period in a UK referral center, ages 28-41 years, with acute or chronic severe hepatocellular injury, poorly responsive to corticosteroids [bilirubin 1.8-30.4 mg/dL, ALT 636-2140 U/L, ANA positive in one]).
  • Stuyt RJ, Willems SM, Wagtmans MJ, van Hoek B. Chewing khat and chronic liver disease. Liver Int 2011; 31: 434-6. [PubMed: 21281438]
    (Report of 6 cases of khat associated liver disease from the Netherlands, all patients from East Africa, some presenting with jaundice and others with portal hypertension and advanced cirrhosis, ages 17-47 years, 6 men and 1 woman [bilirubin 1.2-35.5 mg/dL, ALT 18-1192 U/L, Alk P 42-235 U/L], 4 died).
  • Coton T, Simon F, Oliver M, Kraemer P. Hepatotoxicity of khat chewing. Liver Int 2011; 31: 434. [PubMed: 20825558]
    (Letter in response to Peevers [2010] mentioning that they have never seen liver injury attributable to khat, despite a large population of khat users and analysis of 204 liver biopsies from heavy users in the Djibouti Republic in the Horn of Africa).
  • Douglas H, Boyle M, Lintzeris N. The health impacts of khat: a qualitative study among Somali-Australians. Med J Aust 2011; 195: 666-9. [PubMed: 22171861]
    (Interviews with members of eastern African communities in Australia found that 55% reported khat use, but often did not reveal this to physicians and caregivers).
  • Roelandt P, George C, d'Heygere F, Aerts R, Monbaliu D, Laleman W, Cassiman D, et al. Acute liver failure secondary to khat (Catha edulis)-induced necrotic hepatitis requiring liver transplantation: case report. Transplant Proc 2011; 43: 3493-5. [PubMed: 22099826]
    (26 year old Somalian man with progressive liver failure visiting Belgium from the UK who was a chronic khat user [bilirubin 2.0 rising to 34.1 mg/dL, ALT 372 U/L, Alk P 337 U/L], ultimately undergoing liver transplant).
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    (A systematic compilation of all publications on the hepatotoxicity of specific herbals identified 185 publications on 60 different herbs, herbal drugs, and supplements; does not mention khat or Catha edulis).
  • Bunchorntavakul C, Reddy KR. Review article: herbal and dietary supplement. Aliment Pharmacol Ther 2013; 37: 3-17. [PubMed: 23121117]
    (Systematic review of literature on HDS associated liver injury discusses Chinese and Asian herbs, but does not mention khat or Catha edulis specifically).
  • Forbes MP, Raj AS, Martin J, Lampe G, Powell EE. Khat-associated hepatitis. Med J Aust 2013; 199: 498-9. [PubMed: 24099213]
    (32 year old Somalian man developed jaundice and pruritus and gave a history of khat use for 7 years, recently having changed his supply [bilirubin 14.0 mg/dL, ALT 1880 U/L, Alk P 161 U/L, ANA 1:640], resolving slowly, but with 2 subsequent relapses despite denial of continued khat use).
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    (Review of the frequency and causes of liver test abnormalities in substance abusers, mentions that khat use can cause severe acute and chronic liver injury).
  • Riyaz S, Imran M, Gleeson D, Karajeh MA. Khat (Catha Edulis) as a possible cause of autoimmune hepatitis. World J Hepatol 2014; 6: 150-4. [PMC free article: PMC3959116] [PubMed: 24672645]
    (Among 6 long term users of khat who presented with acute hepatitis between 2005-2010 to a single UK referral center, all were male, ages 24 to 57 years, from Somalia or Yemen and had features of autoimmune hepatitis [5 with liver biopsy], and most responding at least partially to corticosteroid therapy).
  • Navarro VJ, Barnhart H, Bonkovsky HL, Davern T, Fontana RJ, Grant L, Reddy KR, et al. Liver injury from herbals and dietary supplements in the U.S. Drug-Induced Liver Injury Network. Hepatology 2014; 60: 1399-408. [PMC free article: PMC4293199] [PubMed: 25043597]
    (Among 85 cases of HDS associated liver injury [not due to anabolic steroids] enrolled in a US prospective study between 2004 and 2013, the single most commonly implicated herbal agent was green tea extract; no cases were attributed to khat).
  • Pantano F, Tittarelli R, Mannocchi G, Zaami S, Ricci S, Giorgetti R, Terranova D, Busardò FP, Marinelli E. Hepatotoxicity Induced by "the 3Ks": Kava, Kratom and Khat. Int J Mol Sci 2016; 17: 580. [PMC free article: PMC4849036] [PubMed: 27092496]
    (Review of the evidence for hepatotoxicity of kava, kratom and khat mentions the chronic liver injury that resembles an atypical autoimmune hepatitis).
  • Alhaddad OM, Elsabaawy MM, Rewisha EA, Salman TA, Kohla MA, Ehsan NA, Waked IA. Khat-induced liver injuries: A report of two cases. Arab J Gastroenterol 2016; 17: 45-8. [PubMed: 27049456]
    (Two Yemeni men, 31 and 32 years old, with long term daily khat use presented with liver injury [bilirubin 5.4 and 6.1 mg/dL, ALT 400 and 275 U/L, Alk P 273 and 245 U/L, INR 1.1 and 1.4], biopsies showing interface hepatitis and fibrosis, and both improved spontaneously with stopping khat use).
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    (Description of an online compendium of cases of liver toxicity attributed to HDS products does not include listing or discussion of khat).
  • Orlien SMS, Ismael NY, Ahmed TA, Berhe N, Lauritzen T, Roald B, Goldin RD, et al. Unexplained chronic liver disease in Ethiopia: a cross-sectional study. BMC Gastroenterol 2018; 18: 27. [PMC free article: PMC5812015] [PubMed: 29439653]
    (Among 150 patients who presented with chronic liver disease and cirrhosis between 2015-2016 to two hospitals in Ethiopia, the cause was identified in only 67 [45%: HBV in 55, HCV in 2], and khat use was frequent both in the known and unknown etiology groups [84% vs 74%], while alcohol use was rare [9% vs 6%]).
  • Waters M, Oxner A, Krajden S, Sultanian R. Acute liver injury associated with khat use in a 24-year-old male. Case Reports Hepatol. 2018; 2018: 2816907. [PMC free article: PMC6280303] [PubMed: 30584482]
    (24 year old Somalian male Canadian immigrant presented with acute hepatitis of unknown cause [bilirubin 11.1 mg/dL, ALT 2449 U/L, Alk P not given, INR 1.6], which improved during hospitalization without further follow up until 2 months later when he presented with similar injury at which point he was found to have been chewing khat weekly for the previous 3 years: Case 1).
  • Orlien SMS, Berhe NB, Morgan MY, Johannessen A. Khat-related liver disease in sub-Saharan Africa: neglected, yet important. Lancet Glob Health. 2019;7:e310. [PubMed: 30784630]
    (Letter to the editor stressing the importance of khat as a cause of chronic liver disease in sub-Saharan Africa, particularly among men which is often not mentioned in review articles).
  • Vento S, Dzudzor B, Cainelli F, Tachi K. Khat-related liver disease in sub-Saharan Africa: neglected, yet important - Authors' reply. Lancet Glob Health. 2019;7:e311. [PubMed: 30784631]
    (Reply to Orlien et al [2019] mentioning that khat use is highest in Yemen, Somalia, and Eastern Africa, but not particularly common in most Western sub-Saharan countries).
  • Alhaddad O, Elsabaawy M, Abdelsameea E, Abdallah A, Shabaan A, Ehsan N, Elrefaey A, et al. Presentations, causes and outcomes of drug-Induced liver injury in Egypt. Sci Rep. 2020;10(1):5124. [PMC free article: PMC7083870] [PubMed: 32198411]
    (Among 75 cases of drug induced liver injury admitted to a tertiary hospital in Egypt over a one year period, the most common causes were diclofenac [41%], amoxicillin-clavulanate [19%], halothane [11%], ibuprofen (5%], and khat [4%: 3 cases, all hepatocellular and self-limited in course]).
  • Palacios Argueta P, Attar B, Sikavi C, Alagiozian-Angelova V, Mishra S. Drug-induced liver injury caused by "Khat," an herbal stimulant. ACG Case Rep J. 2020;7:e00480. [PMC free article: PMC7721222] [PubMed: 33299901]
    (28 year old Yemeni male immigrant to the US developed jaundice having chewed khat recreationally for 3 years [bilirubin 6.1 mg/dL, ALT 2148 U/L, Alk P 184 U/L, ANA negative, IgG 1490], improving on stopping khat but lost to follow up before liver tests became normal).
  • Malasevskaia I, Al-Awadhi AA, Mohammed L. Tea in the morning and khat afternoon: health threats due to khat chewing. Cureus. 2020;12:e12363. [PMC free article: PMC7842844] [PubMed: 33527046]
    (Review of the history of khat use, its geographic prevalence, and profound effects on both physical and mental health including acute and chronic liver disease and death from cirrhosis).
  • Patel H, Kumar K, Essrani RK, Niazi M, Makker J, Nayudu SK. Acute hepatitis in a Yemeni immigrant associated with khat: a "biological amphetamine" carried in cultures. Clin Pract. 2021;11:167-173. [PMC free article: PMC8006146] [PubMed: 33800126]
    (32 year old Yemeni male who had immigrated to the US one year previously developed abdominal pain and abnormal liver tests [bilirubin 0.7/2.0 mg/dL, ALT 328 U/L, Alk P 78 U/L], admitting to khat use 5-6 times monthly but much less than previously in Yemen, with improvement after stopping and normal liver tests 3 weeks later).
  • Shaikhain G, Gaballah M, Alhazmi A, Khardali I, Hakami A, Oraiby M, Alharbi S, et al. Fatalities involving khat in Jazan, Saudi Arabia, 2018 to 2021. Toxics. 2023;11:506. [PMC free article: PMC10303278] [PubMed: 37368606]
    (Among 651 fatalities undergoing forensic analysis in a Saudi Arabian region over a 4 year period, 30 [5%] had postmortem samples positive for khat, highest levels in urine, the most common causes of death being suicide, homicide, or accident; no mention of hepatic pathology or cirrhosis).

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