Alanine aminotransferase (ALT)
ALT is an enzyme released mostly from liver cells. Upper limits differ: 29 to 35 U/L for men and 19 to 26 for women in guideline and cohort sources, and up to 59 and 41 on one laboratory reference interval. Higher values go with more deaths from liver disease. Results shift between tests, and heavy lifting raises them for days.
- Status
- Part of routine liver and metabolic blood panels, ordered by a clinician and also sold direct to consumers by some US laboratories. FDA classifies ALT test systems as class I devices exempt from premarket notification [1]. Reports print the unit as U/L or IU/L.
- Measures
- The activity of the enzyme alanine aminotransferase in serum or plasma. The enzyme is found mainly in liver tissue, and also in kidney, heart and skeletal muscle [1][2].
- Also called
- ALT, alanine aminotransferase, alanine transaminase, alanine amino transferase, SGPT, serum glutamic pyruvic transaminase, ALAT, GPT, ALT (SGPT), ALT/SGPT
- Tested for
- liver health, fatty liver, hepatitis screening, liver damage from alcohol, liver damage from medication, liver enzymes check
Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on
Linked in research2
Reported risks0
No risks sourced yet.
Reference ranges
Each range is the one its source published, in U/L. Also reported in µkat/L. Where sources differ, each is shown.
American College of Gastroenterology clinical guideline, 2017, men
Adult men · [3]
| Range | What the source calls it |
|---|---|
| 33 or below U/L | "true healthy normal" |
| above 33 U/L | No name given |
The guideline states that a true healthy normal ALT level ranges from 29 to 33 IU/L for males and that levels above this are to be assessed. It gives the upper limit as a range, not one number, and this block places the cut at the top of that range, so a result of 30 to 33 sits above the low end of the guideline's own range. The guideline ties elevated ALT to increased liver-related mortality [3]. Other bodies below publish different limits.
American College of Gastroenterology clinical guideline, 2017, women
Adult women · [3]
| Range | What the source calls it |
|---|---|
| 25 or below U/L | "true healthy normal" |
| above 25 U/L | No name given |
The guideline gives the range as 19 to 25 IU/L for females. This block places the cut at the top of that range, so a result of 20 to 25 sits above the low end of the guideline's own range [3].
American Association for the Study of Liver Diseases hepatitis B guidance, 2018, men
Males with chronic hepatitis B, for treatment decisions · [4]
| Range | What the source calls it |
|---|---|
| 35 or below U/L | "normal" |
| above 35 U/L | "elevated" |
The guidance reports that upper limits of normal in healthy adults are 29 to 33 U/L for males, then sets 35 U/L for males to guide the management of chronic hepatitis B, to be used in place of the local laboratory's limit. It notes that repeat testing of the same sample can give different results. The cut point was set for hepatitis B treatment decisions, not as a general population interval [4].
American Association for the Study of Liver Diseases hepatitis B guidance, 2018, women
Females with chronic hepatitis B, for treatment decisions · [4]
| Range | What the source calls it |
|---|---|
| 25 or below U/L | "normal" |
| above 25 U/L | "elevated" |
The guidance reports upper limits of 19 to 25 U/L in healthy adult females and sets 25 U/L for females to guide the management of chronic hepatitis B. It treats more than twice the limit (above 50 U/L for women, above 70 U/L for men) as a separate treatment threshold [4].
Prati and colleagues, Italian blood donor cohort, 2002, men
Adult men, from first-time blood donors at lowest risk of liver disease · [5]
| Range | What the source calls it |
|---|---|
| 30 or below U/L | "healthy range" |
| above 30 U/L | No name given |
Computed from 6,835 first-time blood donors in Milan, using the group at lowest risk for liver disease. The authors compared this limit with the 40 U/L then in use for men. Against it, sensitivity for detecting hepatitis C viremia rose from 55% to 76.3% and specificity fell from 97.4% to 88.5% [5].
Prati and colleagues, Italian blood donor cohort, 2002, women
Adult women, from first-time blood donors at lowest risk of liver disease · [5]
| Range | What the source calls it |
|---|---|
| 19 or below U/L | "healthy range" |
| above 19 U/L | No name given |
The authors compared this limit with the 30 U/L then in use for women. Set from one Italian center [5].
Ruhl and Everhart, US national survey, 2012, men
Adult men in the US National Health and Nutrition Examination Survey, 1999 to 2008 · [6]
| Range | What the source calls it |
|---|---|
| 29 or below U/L | No name given |
| above 29 U/L | "elevated" |
The cut point is the one that most often classified men correctly as either positive for hepatitis C virus RNA or at low risk of liver injury (88% sensitivity, 83% specificity). At this cut point 36.4% of US men would have had an abnormal ALT. The 95th percentile of low-risk men was 44 IU/L, and the authors describe that higher limit as preferable when ALT is not needed to find hepatitis C. The authors call for further testing of any limit in other populations [6].
Ruhl and Everhart, US national survey, 2012, women
Adult women in the US National Health and Nutrition Examination Survey, 1999 to 2008 · [6]
| Range | What the source calls it |
|---|---|
| 22 or below U/L | No name given |
| above 22 U/L | "elevated" |
Set the same way as for men (89% sensitivity, 82% specificity). At this cut point 28.3% of US women would have had an abnormal ALT. The 95th percentile of low-risk women was 32 IU/L [6].
Lee and colleagues, Korean liver donor cohort, 2010, men
Adult men, from potential liver donors with normal liver biopsies · [7]
| Range | What the source calls it |
|---|---|
| 35 or below U/L | "healthy" |
| above 35 U/L | No name given |
Calculated from 643 Korean men with biopsy-proven normal livers, median age 25 and median body mass index 22.3. The abstract gives 35 IU/L as the threshold without stating which side a result of exactly 35 falls on, and this block treats it as an upper limit. Age and body mass index were independently related to ALT even in people with normal livers [7].
Lee and colleagues, Korean liver donor cohort, 2010, women
Adult women, from potential liver donors with normal liver biopsies · [7]
| Range | What the source calls it |
|---|---|
| 26 or below U/L | "healthy" |
| above 26 U/L | No name given |
Calculated from 462 Korean women with biopsy-proven normal livers, median age 30 and median body mass index 21.4. The abstract gives 26 IU/L as the threshold without stating which side a result of exactly 26 falls on [7].
International Federation of Clinical Chemistry multicenter study, 2010, women
Adult women aged 18 to 85 · [8]
| Range | What the source calls it |
|---|---|
| below 8 U/L | No name given |
| 8 to 41 U/L | "reference interval" |
| above 41 U/L | No name given |
A laboratory reference interval, the central 95% of results in selected people, not a cut point set for a disease outcome. From 765 individuals in Italy, China, Turkey and the Nordic countries, measured on systems standardized to the federation's reference measurement systems. Results did not differ between regions [8].
International Federation of Clinical Chemistry multicenter study, 2010, men
Adult men aged 18 to 85 · [8]
| Range | What the source calls it |
|---|---|
| below 9 U/L | No name given |
| 9 to 59 U/L | "reference interval" |
| above 59 U/L | No name given |
A laboratory reference interval from the same study, 354 men among 765 individuals. Its upper limit is about twice the limits the liver societies publish above [8].
US national survey laboratory procedure manual, 2017 to 2018, women
Adult women, as the reference range printed for the assay · [2]
| Range | What the source calls it |
|---|---|
| 0 to 31 U/L | "reference range" |
| above 31 U/L | No name given |
The reference range listed in the laboratory manual for the method used in the 2017 to 2018 US National Health and Nutrition Examination Survey (Roche Cobas 6000), standardized against the international federation's formulation. It is the range attached to that assay, not one derived from survey participants [2].
US national survey laboratory procedure manual, 2017 to 2018, men
Adult men, as the reference range printed for the assay · [2]
| Range | What the source calls it |
|---|---|
| 0 to 40 U/L | "reference range" |
| above 40 U/L | No name given |
From the same manual and method as the range for women [2].
American Board of Internal Medicine laboratory reference ranges, 2026
Adults, both sexes, as the range printed for board examinations · [9]
| Range | What the source calls it |
|---|---|
| below 10 U/L | No name given |
| 10 to 40 U/L | "reference range" |
| above 40 U/L | No name given |
One range for both sexes, published as a reference table for examination candidates. The table does not say how the range was set [9].
What has been shown to move it
Shown to lower it8
Liver enzymes in fatty liver disease
Shown to lower liver enzymes in fatty liver disease, ALT by about 9 U/L. Liver fat and scarring were not measured.
The numbers and sources
- Effect
- In people with metabolic dysfunction-associated steatotic liver disease, orlistat lowered AST by 4.01 U/L (95% CI 1.97 to 6.05), ALT by 8.70 U/L (95% CI 0.90 to 16.51) and GGT by 7.74 U/L (95% CI 0.59 to 14.88) against control. LDL cholesterol fell 5.61 mg/dL, fasting glucose 4.05 mg/dL, HOMA-IR 0.70 and BMI 0.99 kg/m². Blood pressure did not change [6]. A second meta-analysis also found lower ALT, AST, HOMA-IR, BMI, cholesterol, insulin and waist circumference [7].
- Population
- 6 RCTs [6]; 11 studies with 582 participants [7].
- Sources
- [6], [7]
- Caveats
- Both reviews measured blood markers, not liver fat on imaging or scarring on biopsy. The trials were small and likely overlap between the reviews. The abstract of [7] does not say whether all 11 studies were randomized.
Liver enzymes and lipids in fatty liver disease (quercetin alone)
Shown to lower liver enzymes, LDL and triglycerides with quercetin alone in people with fatty liver disease, at very low to moderate certainty.
The numbers and sources
- Effect
- A 2025 meta-analysis of 7 RCTs (540 patients) with metabolic dysfunction-associated steatotic liver disease found that quercetin lowered ALT, AST, GGT, direct bilirubin and C-reactive protein, lowered total cholesterol, LDL and triglycerides, and raised HDL. BMI, body fat, kidney function and TNF-α did not change [10].
- Population
- 540 patients with fatty liver disease in 7 RCTs [10].
- Sources
- [10]
- Caveats
- GRADE certainty ranged from very low to moderate. Dose, baseline BMI and age may explain heterogeneity. The abstract gives no pooled effect sizes [10]. None of the trials measured senescent cells.
Fatty liver disease
Shown to lower liver enzymes in fatty liver disease, ALT by about 7 to 12 U/L, with low certainty and no data on deaths.
The numbers and sources
- Effect
- In 26 trials (2,375 patients), silymarin lowered ALT (pooled difference -12.39, 95% CI -19.69 to -5.08) and AST (-10.97, 95% CI -15.51 to -6.43), lowered total cholesterol, triglycerides and LDL, and improved steatosis on histology (OR 3.25, 95% CI 1.80 to 5.87) [5]. In a 48-week biopsy trial of 99 adults with NASH, a 30% or greater fall in disease activity score occurred in 32.7% on 700 mg three times a day and 26.0% on placebo (p 0.467). Fibrosis fell by 1 point or more in 22.4% against 6.0% (p 0.023) [6]. A 2025 Cochrane review of 17 RCTs (2,069 adults) found silymarin alone against placebo or no treatment may lower ALT by 7.21 U/L (95% CI -10.62 to -3.80, 6 trials, very low certainty). Silymarin complexes did not lower ALT, and no trial reported deaths or quality of life [7]. In a 2025 meta-analysis of 25 studies (2,283 patients), silymarin alone lowered LDL cholesterol (SMD -0.25), while ALT fell when silymarin was combined with diet or lifestyle change [8].
- Population
- Adults with fatty liver disease [5][7][8]. 99 adults with biopsy-proven NASH in Malaysia [6].
- Sources
- [5], [6], [7], [8]
- Caveats
- The meta-analysis authors state that the effects need confirmation [5]. The biopsy trial missed its primary outcome, and its fibrosis finding was secondary [6]. The Cochrane authors rated the evidence low to very low certainty and called benefits and harms unclear [7].
Muscle and physical function
Mixed results: one review found no change in muscle mass, strength or gait speed in older adults, while others found better endurance or gait speed.
A 2025 meta-analysis of 9 RCTs (412 middle-aged and older adults) found faster gait speed on NMN (SMD 0.34, 95% CI 0.03 to 0.66) and lower ALT (SMD -0.29, 95% CI -0.55 to -0.03).
The numbers and sources
- Effect
- In adults with a mean age over 60, NMN did not change skeletal muscle index (MD -0.42, 95% CI -0.99 to 0.14), grip strength, gait speed (MD -0.01 m/s, 95% CI -0.08 to 0.06) or chair-stand time. Knee extension strength, SPPB scores and thigh muscle mass did not improve [4]. A network meta-analysis of NAD precursors reported higher endurance with NMN at medium dose (SMD 0.66, 95% CI 0.09 to 1.23) and high dose (SMD 1.02, 95% CI 0.43 to 1.60), with no change in strength [5]. One trial reported a longer six-minute walk on 300 to 900 mg a day than placebo [1]. A 2025 meta-analysis of 9 RCTs (412 middle-aged and older adults) found faster gait speed on NMN (SMD 0.34, 95% CI 0.03 to 0.66) and lower ALT (SMD -0.29, 95% CI -0.55 to -0.03) [6].
- Population
- Randomized trials in adults with mean ages of 60.9 to 83 years [4]; 27 studies with 1,599 adults across NR, NMN, NADH and nicotinamide [5]; 80 middle-aged adults [1]; 412 middle-aged and older adults [6].
- Sources
- [4], [5], [1], [6]
- Caveats
- The reviews disagree on endurance and on gait speed [4][5][6]. The pooled muscle analysis included 2 to 5 studies per measure [4]. The network analysis mixes precursors and populations [5].
Liver tests
Raised liver tests were about as common on orforglipron as on comparators across phase 3 trials, and other causes accounted for every serious case.
The numbers and sources
- How common
- Uncommon: between 1 in 1,000 and 1 in 100 people.
- Effect
- Across seven phase 3 trials, mean ALT and AST fell on orforglipron, and raised levels occurred at similar rates on orforglipron and comparators. Six people (0.1%) in each group had ALT or AST at 3 or more times the upper limit with bilirubin at 2 or more times, and other causes accounted for every orforglipron case [13].
- Population
- 11,220 participants, 6,920 on orforglipron, for up to 104 weeks [13].
- Sources
- [13]
- Caveats
- A pooled analysis by the manufacturer's investigators. The trials excluded people with markedly raised liver enzymes at screening [13].
Fatty liver and liver enzymes
Shown to lower the liver enzymes ALT and AST slightly in adults with fatty liver disease, but not in people with diabetes or with piperine added.
The numbers and sources
- Effect
- In 15 RCTs (905 patients with nonalcoholic fatty liver disease), curcumin lowered ALT by 4.10 (95% CI -7.16 to -1.04) and AST by 3.27 (95% CI -5.16 to -1.39), with no change in ALP. Curcumin with piperine did not change ALT or AST significantly [36]. In 10 RCTs in prediabetes and diabetes, ALT and AST did not change significantly and GGT fell 2.35 IU/L [37]. Across 18 RCTs of curcuminoids with piperine, AST fell 2.29 IU and the ALT change was not significant (p 0.053) [18].
- Population
- Adults with nonalcoholic fatty liver disease [36]; adults with prediabetes or diabetes [37]; adults in curcumin with piperine trials [18].
- Sources
- [36], [37], [18]
- Caveats
- These are blood enzymes, not measures of liver fat or fibrosis. Results differed by population and formulation [36][37].
Fatty liver inflammation (NASH)
Shown to improve liver inflammation in adults with NASH without diabetes, 43% against 19% on placebo in one trial. Results on fibrosis disagree.
Across 3 placebo-controlled RCTs in steatohepatitis, vitamin E lowered ALT (MD -12.27, 95% CI -16.66 to -7.89) and raised the odds of fibrosis improvement (OR 1.96, 95% CI 1.25 to 3.09).
The numbers and sources
- Effect
- After 96 weeks, nonalcoholic steatohepatitis improved in 43% on 800 IU a day and 19% on placebo. Liver enzymes, fat and inflammation fell. Fibrosis scores did not improve [6]. Across 3 placebo-controlled RCTs in steatohepatitis, vitamin E lowered ALT (MD -12.27, 95% CI -16.66 to -7.89) and raised the odds of fibrosis improvement (OR 1.96, 95% CI 1.25 to 3.09). Resolution of steatohepatitis did not differ significantly (OR 1.71, 95% CI 0.69 to 4.27) [7]. Across 16 RCTs in fatty liver disease, vitamin E lowered AST (WMD -5.94 IU/L) and ALT (WMD -7.33 IU/L) [8]. In a Chinese trial, liver histology improved in 29.3% on 300 mg a day and 14.1% on placebo, with gains in steatosis, inflammation and fibrosis stage [9].
- Population
- 247 adults with nonalcoholic steatohepatitis and without diabetes [6]; adults with steatohepatitis in 2 US trials and 1 Chinese trial [7]; adults with metabolic dysfunction-associated steatotic liver disease [8]; 124 adults without diabetes with biopsy-proven steatohepatitis in China [9].
- Sources
- [6], [7], [8], [9]
- Caveats
- The 3-trial review is small and its resolution result was heterogeneous [7]. The first large trial found no fibrosis improvement [6], while the pooled analysis and the Chinese trial did [7][9]. The enzyme review could not judge fibrosis or long-term liver outcomes [8].
Liver function in chronic hepatitis B
One trial without placebo found lower ALT when glutathione was added to entecavir for 3 months in chronic hepatitis B.
The numbers and sources
- Effect
- In one trial, reduced glutathione added to entecavir for 3 months lowered ALT to 31.11 U/L against 56.90 U/L on entecavir alone, from about 348 U/L in both groups. Fibrosis markers fell more, and HBV DNA was undetectable at 48 weeks in 68.89% against 42.22% [10].
- Population
- 90 patients with chronic hepatitis B [10].
- Sources
- [10]
- Caveats
- One trial without placebo. The abstract does not state the glutathione dose or route [10].
Shown to raise it15
Liver enzyme elevation
Shown to raise liver enzymes, about 6 times the odds on placebo, mostly at high doses or with antiepileptic drugs. No cases appeared under 300 mg a day in adults.
In an FDA-run trial of 201 healthy adults, 5 mg/kg a day for 28 days raised ALT or AST above 3 times normal in 5.6% on CBD and 0% on placebo, with increased eosinophilia.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- Across 12 placebo-controlled trials (1,229 participants), CBD raised the odds of liver enzyme elevation (OR 5.85, 95% CI 3.84 to 8.92) and drug-induced liver injury (OR 4.82, 95% CI 2.46 to 9.45). In 28 trials, the pooled rate of enzyme elevation was 7.4% and of liver injury 3.0%. High dose (1,000 mg a day or more, or 20 mg/kg or more) and use with antiepileptic drugs were risk factors. No cases were reported in adults under 300 mg a day, and no severe injury was reported [12]. In an FDA-run trial of 201 healthy adults, 5 mg/kg a day for 28 days raised ALT or AST above 3 times normal in 5.6% on CBD and 0% on placebo, with increased eosinophilia [11]. In the Lennox-Gastaut trial, 9% of CBD patients had raised aminotransferases [2].
- Population
- Trial participants with epilepsy and healthy adults [2][11][12].
- Sources
- [2], [11], [12]
- Caveats
- In the healthy-adult trial, elevations meeting withdrawal criteria were found at day 21 in 2 people and day 28 in 5 [11]. Long-term effects at lower consumer doses were not measured [11].
Raised liver enzymes at 4 g a day
Shown to raise liver enzymes, with abnormal liver tests in 7.0% on paracetamol against 1.8% on placebo in osteoarthritis trials.
In healthy adults given 4 g a day in a controlled inpatient setting, ALT rose above 3 times the upper limit of normal in 31% to 44% of the 4 acetaminophen groups and in none of 39 on placebo.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- In the osteoarthritis trials, abnormal liver function tests occurred in 70 per 1,000 on paracetamol and 18 per 1,000 on placebo (RR 3.79, 95% CI 1.94 to 7.39) [8]. In healthy adults given 4 g a day in a controlled inpatient setting, ALT rose above 3 times the upper limit of normal in 31% to 44% of the 4 acetaminophen groups and in none of 39 on placebo. Median peak ALT was 2.78 times that on placebo (95% CI 1.47 to 4.09) [20].
- Population
- 3,541 people with osteoarthritis in 10 trials [8]; 145 healthy adults, 106 on acetaminophen alone or with an opioid and 39 on placebo, for an intended 14 days [20].
- Sources
- [8], [20]
- Caveats
- The reviewers called the clinical importance of the enzyme rises uncertain [8]. The band here is taken from the pooled 7.0%. The healthy-volunteer trial was single-blind [20].
Raised liver enzymes on quetiapine
Shown to raise the liver enzyme ALT in 5% on quetiapine against 1% on placebo in schizophrenia and mania trials.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- In trials of 3 to 12 weeks, increased ALT was reported in 5% on quetiapine and 1% on placebo, and increased AST in 3% against 1% [3].
- Population
- 719 people on quetiapine and 404 on placebo [3].
- Sources
- [3]
- Caveats
- Reported as adverse reactions in short trials, with no data here on how long the rises lasted. The evidence is for quetiapine.
Liver toxicity
Shown to raise blood test signs of liver toxicity in 6% of women in one trial. French case reports include one liver transplant and two likely deaths.
ALT exceeded 10 times normal in 68%, 41% were hospitalized, one needed a liver transplant and two others likely died of liver failure.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- In the US trial, 6% of women had blood test evidence of liver toxicity on coumarin [3]. A French pharmacovigilance survey reviewed 34 cases of raised liver enzymes up to June 1996 and judged 15 likely or probably caused by coumarin. ALT exceeded 10 times normal in 68%, 41% were hospitalized, one needed a liver transplant and two others likely died of liver failure [5]. A woman in Sri Lanka developed abnormal liver tests on Lympedim that led to stopping the drug [6]. A risk assessment found that clinical data reveal a subgroup of people more susceptible to coumarin's liver toxicity than the animals studied, and derived a tolerable daily intake of 0.1 mg per kg of body weight [7].
- Population
- 140 women in an RCT [3]. Case reports to French regional centers and the manufacturer [5]. A single case [6].
- Sources
- [3], [5], [6], [7]
- Caveats
- Most French cases occurred 2 to 6 months into treatment at about 90 mg a day [5]. The cause of the higher susceptibility in some people is not known [7].
Fenofibrate: liver enzymes and liver injury
Shown to raise ALT above 3 times normal in 5.3% against 1.1% on placebo. The label warns of serious liver injury after approval, including transplant and death.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- In 10 placebo-controlled trials, ALT rose above 3 times the upper limit in 5.3% on fenofibrate and 1.1% on placebo. In label trials, increased AST was 3.4% against 0.5% and abnormal liver tests 7.5% against 1.4%, and raised liver tests caused 1.6% to stop. In an 8-week study, ALT or AST rises of 3 times or more reached 13% at the higher doses. The label reports serious drug-induced liver injury after approval [7].
- Population
- 439 people on fenofibrate and 365 on placebo, and a pooled 10-trial analysis [7].
- Sources
- [7]
- Caveats
- Postmarketing liver injury reports have no denominator.
Liver enzyme rises
Shown to raise ALT or AST to 3 times normal or more in about 1% of women on Oriahnn and under 1% on Myfembree, against 0% to 0.4% on placebo.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- ALT rose to 3 times the upper limit or more in 1.1% (4 of 379) on Oriahnn and AST in 1.3% (5 of 379), against none on placebo, peaking at 8 and 6 times the limit, and returning to baseline within 4 months [6]. On Myfembree in fibroid trials, ALT rose in 0.4% (1 of 254) and AST in 0.8% (2 of 254), against 0% and 0.4% on placebo [2]. On leuprolide, 3% of women with fibroids had post-treatment transaminases at least twice baseline and above normal [10].
- Population
- Premenopausal women with fibroids in the placebo-controlled trials [2][6][10].
- Sources
- [6], [2], [10]
- Caveats
- Few events. Both labels contraindicate use in liver disease [2][6].
Raised liver enzymes
Shown to raise liver enzymes mildly to moderately in about 15% of people in trials. The label also reports clinical hepatitis.
ALT, AST, GGT and alkaline phosphatase are among the tests the label lists as increased.
The numbers and sources
- How common
- Very common: more than 1 in 10 people.
- Effect
- Mild to moderate rises in liver enzymes were seen in about 15% of people in clinical trials, some returning to normal with a lower dose or continued treatment. ALT, AST, GGT and alkaline phosphatase are among the tests the label lists as increased [3]. A meta-analysis found statistically significant changes in hepatic panel means, with ALT averaging 21.77 U/L and AST 22.67 U/L during treatment, and few results outside the normal range [9]. Elevated liver enzymes led to withdrawal from trials in some [1].
- Population
- Isotretinoin capsule trials [3]; 1,574 patients in 26 studies [9]; 760 people in 11 trials [1].
- Sources
- [3], [9], [1]
- Caveats
- The meta-analysis authors concluded that monthly laboratory testing is not supported for standard doses in the standard patient [9].
Raised liver enzymes
Shown to raise the liver enzyme ALT to three times the normal limit or more in 2.0% against 0.3% on placebo in short trials.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- ALT rose to at least three times the upper limit of normal in 2.0% (8 of 424) on mirtazapine and 0.3% (1 of 328) on placebo. Some people stopped the drug, and in others levels returned to normal while it was continued [7].
- Population
- 424 adults on mirtazapine and 328 on placebo in short-term US trials [7].
- Sources
- [7]
- Caveats
- Short trials, with no rate of liver injury given.
Liver injury
Shown to raise liver enzymes on duloxetine, with ALT above 3 times the upper limit in 1.25% against 0.45% on placebo. Liver failure has been reported.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- In adult placebo-controlled duloxetine trials, ALT rose above 3 times the upper limit of normal in 1.25% (144 of 11,496) on duloxetine and 0.45% (39 of 8,716) on placebo, with a dose-response relationship in fixed-dose studies. Liver enzyme rises led 0.3% (92 of 34,756) to stop the drug. The label also reports cases of hepatic failure, some fatal, and cholestatic jaundice [18].
- Population
- Adults in duloxetine clinical trials for any indication, and postmarketing reports [18].
- Sources
- [18]
- Caveats
- The evidence in this block is for duloxetine only. The serious cases come from reports with no denominator.
Liver enzyme rises and liver injury
Shown to raise the liver enzyme ALT above twice the reference limit in 1.9% on glimepiride against 0.8% on placebo. Liver failure appears in postmarketing reports.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- In 11 pooled placebo-controlled trials, 1.9% on glimepiride and 0.8% on placebo developed serum ALT above 2 times the upper reference limit. Postmarketing reports include impaired liver function with cholestasis and jaundice, and hepatitis that may progress to liver failure [3]. The glyburide label states that liver enzyme elevations were more frequent when glyburide was taken with bosentan, and lists the combination as contraindicated [14].
- Population
- 745 people on glimepiride and 294 on placebo in 11 trials [3].
- Sources
- [3], [14]
- Caveats
- Postmarketing reports have no denominator.
Liver enzymes and liver injury
The label reports rises in AST, ALT and alkaline phosphatase in 1% or more of people, and cases of reversible liver injury.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- The label lists increases in AST, ALT and alkaline phosphatase among reactions occurring in 1% or more, and states that cases of reversible liver injury have occurred, with hepatic necrosis and granulomatous hepatitis reported in under 1% [5]. In a dose-escalation trial, mild rises in liver tests were frequent in both the escalation and control groups [3].
- Population
- People taking allopurinol, as described in the label [5]; 183 people with gout [3].
- Sources
- [5], [3]
- Caveats
- The label gives no placebo rate and no size for the enzyme rises.
Liver enzyme and muscle taurine changes
Limited evidence: ALT rose slightly but stayed within reference ranges, and muscle taurine did not change in humans.
The numbers and sources
- How common
- How often is not known: the sources give no rate.
- Effect
- Beta-alanine raised circulating alanine aminotransferase slightly (effect size 0.274, 95% CrI 0.04 to 0.527), with mean values within clinical reference ranges. Muscle taurine (0.156, 95% CrI -0.38 to 0.72) and histidine did not change in humans. Taurine fell in mice only at 3% or more beta-alanine in drinking water [9].
- Population
- 101 human and 50 animal studies [9].
- Sources
- [9]
- Caveats
- The abstract does not report trial durations. No trials of use over years were located.
Raised ALT liver enzyme from unfiltered coffee
Small trials found unfiltered coffee raised the liver enzyme ALT. In one, 8 of 22 people drinking 5 to 6 strong cups of French press coffee exceeded the normal limit.
The numbers and sources
- How common
- Very common: more than 1 in 10 people.
- Effect
- Against filtered coffee, cafetière coffee raised alanine aminotransferase by up to 80%, and by 45% (9 U/L, 95% CI 3 to 15) after 24 weeks. ALT exceeded the upper limit of normal in 8 of 22 people on cafetière coffee, twice the limit in 3. The abstract gives no count for the filtered coffee group. All rises reversed after stopping [18]. Eating 8 g of fine coffee grounds a day for 3 weeks raised ALT by 18 U/L (95% CI 4 to 32) against controls [21].
- Population
- 46 adults, 22 on cafetière coffee and 24 on filtered coffee [18]. 14 volunteers in a parallel study and 15 in a crossover [21].
- Sources
- [18], [21]
- Caveats
- Small trials of high intakes of unfiltered coffee. Cohorts of all coffee types link coffee to lower liver disease (see Outcomes).
Raised liver enzymes
The label reports ALT or AST above twice the upper limit in 1% to 2% of patients on ondansetron with chemotherapy, transient, with chemotherapy's role unclear.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- AST or ALT exceeded twice the upper limit of normal in about 1% to 2% of 723 patients receiving ondansetron with cyclophosphamide-based chemotherapy. The rises were transient and not related to dose or duration, and symptomatic liver disease did not occur. Liver failure and death have been reported in cancer patients also taking liver-toxic drugs [3].
- Population
- 723 patients in US chemotherapy trials [3].
- Sources
- [3]
- Caveats
- No placebo rate is given, and the label states the role of chemotherapy is unclear [3].
Liver disease and liver injury
The label warns that drugs acting on GABA receptors have been associated with hepatic encephalopathy in people with liver failure, and lists postmarketing reports of liver injury.
In the trial database, abnormal liver function and raised ALT were listed as infrequent, between 1 in 100 and 1 in 1,000.
The numbers and sources
- How common
- How often is not known: the sources give no rate.
- Effect
- The label states that people with liver impairment clear zolpidem more slowly, and that drugs affecting GABA receptors have been associated with precipitating hepatic encephalopathy in people with hepatic insufficiency. Postmarketing reports include acute hepatocellular, cholestatic or mixed liver injury with or without jaundice. In the trial database, abnormal liver function and raised ALT were listed as infrequent, between 1 in 100 and 1 in 1,000 [13].
- Population
- Postmarketing reports and 3,660 people in preapproval trials [13].
- Sources
- [13]
- Caveats
- The label states that events in the trial database were not necessarily caused by zolpidem, and gives no placebo rate.
Studies disagree2
Alcohol-related and viral liver disease
Not shown to lower deaths or liver complications in alcohol-related or viral liver disease. Results on liver enzymes disagreed.
In 154 people with hepatitis C, 420 or 700 mg three times a day for 24 weeks did not lower ALT more than placebo.
The numbers and sources
- Effect
- Across 18 trials (1,088 patients), milk thistle did not significantly change all-cause mortality (RR 0.78, 95% CI 0.53 to 1.15), complications of liver disease (RR 0.95, 95% CI 0.83 to 1.09) or liver histology. Liver-related mortality was lower across all trials (RR 0.50, 95% CI 0.29 to 0.88) but not in the high-quality trials (RR 0.57, 95% CI 0.28 to 1.19) [1]. In 154 people with hepatitis C, 420 or 700 mg three times a day for 24 weeks did not lower ALT more than placebo. Two people in each group met the primary goal, and viral load and quality of life did not differ [2]. Reviews of liver enzymes in alcohol-related disease disagree. Across 15 RCTs (1,221 patients), silibinin capsules lowered ALT (SMD -1.16) and AST (SMD -1.56) [3]. A meta-analysis of 55 trials (3,545 patients) found no significant effect on AST or ALT in the alcohol-related liver disease subgroup [4].
- Population
- Adults with alcoholic liver disease or hepatitis B or C [1]. 154 adults in the US with hepatitis C not cleared by interferon [2]. Adults with alcohol-related liver disease [3]; adults with liver injury of several causes [4].
- Sources
- [1], [2], [3], [4]
- Caveats
- Only 28.6% of the Cochrane trials reported high methodological quality characteristics [1]. Enzyme changes are surrogate measures, and [3] did not report deaths.
Raised liver enzymes with trazodone
Mixed results: one report linked buspirone taken with trazodone to liver enzyme rises of 3 to 6 times in a few patients, and a repeat study did not.
The numbers and sources
- How common
- How often is not known: the sources give no rate.
- Effect
- The label describes one report suggesting that taking trazodone and buspirone together may have caused 3-fold to 6-fold elevations in the liver enzyme ALT in a few patients. A similar study attempting to replicate the finding identified no effect on liver enzymes [4].
- Population
- A few patients in one report, and a follow-up study, both summarized in labeling [4].
- Sources
- [4]
- Caveats
- One unreplicated report. The label gives no numbers.
Tested, and not shown to change it5
Liver and kidney markers in trials
Liver and kidney markers did not worsen in most trials. Creatinine rose slightly in 3 trials, and doses above 2,000 mg a day were linked to a BUN change.
The numbers and sources
- How common
- How often is not known: the sources give no rate.
- Effect
- In 19 trials (1,295 participants), Nigella sativa lowered ALP by 10.8 U/L and BUN by 1.016. Creatinine rose by 0.070 in 3 trials with covariate-adjusted analyses, and doses above 2,000 mg a day were linked to a BUN change in 2 trials [11]. In 70 healthy adults given 200 mg a day of a thymoquinone-rich oil for 90 days, liver and kidney tests did not change and no serious adverse effects were reported [12].
- Population
- Adults in RCTs [11]. 70 healthy adults [12].
- Sources
- [11], [12]
- Caveats
- The safety trial's corresponding author is at Akay Natural Ingredients, the maker of the tested oil [12]. Heterogeneity for ALP and BUN was high [11]. In 16 RCTs in type 2 diabetes, AST, ALT and creatinine did not change significantly [7].
Liver enzymes
ALT and AST did not change with CLA against control across 22 trials.
Liver enzymes
Liver enzymes did not change significantly across 16 controlled trials. Alkaline phosphatase fell at doses above 1 g a day.
The numbers and sources
- How common
- How often is not known: the sources give no rate.
- Effect
- A 2026 meta-analysis of 16 controlled trials (1,171 participants) found no significant change in ALT (-1.41 IU/L, 95% CI -3.07 to 0.26), AST (0.03 IU/L, 95% CI -0.12 to 0.18) or alkaline phosphatase (SMD -0.21, 95% CI -0.44 to 0.03). Alkaline phosphatase fell at doses above 1 g a day [10].
- Population
- Participants in 16 controlled clinical trials [10].
- Sources
- [10]
- Caveats
- Liver enzymes are a marker, not a count of liver injury. The authors call for trials in more uniform populations [10].
Liver enzymes and side effects in trials
Liver enzymes did not change in short trials. In one trial, gut side effects were twice as common as on placebo.
The numbers and sources
- How common
- How often is not known: the sources give no rate.
- Effect
- In pooled trials, garcinia did not change ALT (Hedges' g 0.27, 95% CI -0.20 to 0.73) or AST (Hedges' g -0.08, 95% CI -0.43 to 0.26) [6]. In one trial included in [1], gastrointestinal adverse events were twice as common with hydroxycitric acid as with placebo [1].
- Population
- 444 participants in 9 publications [6]; RCTs [1].
- Sources
- [1], [6]
- Caveats
- Trials were short and too small to detect rare liver injury. The registry and case findings [7][8][9][10] and the trial enzyme data describe different things.
Liver enzyme changes
Shown to raise mean GGT and alkaline phosphatase in placebo-controlled trials, mostly within the normal range. ALT and AST did not differ.
ALT, AST, albumin and total bilirubin did not differ. "Abnormal liver function" was reported as an adverse reaction in 2% vs 1% on placebo.
The numbers and sources
- How common
- Common: between 1 in 100 and 1 in 10 people.
- Effect
- Mean GGT and alkaline phosphatase were higher after modafinil but not placebo, and rose over time, with few values outside the normal range. ALT, AST, albumin and total bilirubin did not differ. "Abnormal liver function" was reported as an adverse reaction in 2% vs 1% on placebo [3].
- Population
- Adults in placebo-controlled label trials [3].
- Sources
- [3]
- Caveats
- The label gives no size for the mean change. The band above is the adverse-reaction rate.
How it compares with the reference method
Mixed results3
Finding fatty liver disease
Shown to miss part of fatty liver disease: in pooled studies 25% of people with nonalcoholic fatty liver disease had a normal ALT.
The numbers and sources
- Compared with
- Nonalcoholic fatty liver disease or steatohepatitis diagnosed by imaging or biopsy
- Effect
- In a meta-analysis of 11 studies, 25% of people with nonalcoholic fatty liver disease had a normal ALT (95% CI 20 to 31), as did 19% of people with nonalcoholic steatohepatitis (95% CI 13 to 27) [16]. How many are missed depends on the limit used. In Italian blood donors, lowering the limit from 40 to 30 U/L for men and from 30 to 19 U/L for women raised sensitivity for hepatitis C viremia from 55% to 76.3% and lowered specificity from 97.4% to 88.5% [5].
- Population
- 4,084 patients in 11 studies [16]. 6,835 blood donors and 209 people with hepatitis C antibodies [5].
- Sources
- [16], [5]
- Caveats
- The pooled studies used different definitions of a normal ALT, and the authors state no threshold for acceptable performance, so the result is given as numbers only [16].
Variation from one test to the next
Shown to vary between tests: 31% of US adults with a raised ALT had a normal result when retested about 17 days later.
The numbers and sources
- Compared with
- A repeat measurement in the same person
- Effect
- Among 1,864 US adults measured twice a mean of 17.5 days apart, 31% of those with an initially elevated ALT had a normal result the second time, and more than 95% of initially normal results stayed normal. The within-person coefficient of variation was 20.4% [17]. In 91 healthy Europeans sampled weekly for 10 weeks under a tightly controlled protocol, within-person biological variation was 9.3% and variation between people was 28.2% [18].
- Population
- 1,864 adults in the third US National Health and Nutrition Examination Survey [17]. 91 healthy adults aged 21 to 69 at 6 European laboratories [18].
- Sources
- [17], [18]
- Caveats
- The US study had only 2 measurements per person and lacked a full liver disease history [17]. The two studies differ in design, which may explain the gap between 20.4% and 9.3%. Neither states a threshold for agreement.
Differences between laboratories
One statewide survey found the upper limit printed for ALT varied widely between laboratories, mostly because analyzer makers supply different reference intervals.
The numbers and sources
- Compared with
- The upper limits and analyzer results of other laboratories in the same state
- Effect
- In a survey of Indiana laboratories, the upper limit of normal for ALT varied widely for both men and women. Results for the same 5 proficiency samples differed between analyzer brands by an amount that was statistically significant and that the authors judged not clinically significant. Most laboratories took their limit from the analyzer maker, and 17% tested their own volunteers [19]. An international study that standardized its methods found one reference interval could be shared across 4 regions [8].
- Population
- 108 eligible laboratories in Indiana, of which 62% responded [19].
- Sources
- [19], [8]
- Caveats
- One US state, published in 2009. The abstract gives no figures for the spread of limits [19].
Did not match the reference method1
Heavy exercise and muscle injury
Small studies found ALT rose for at least 7 days after one weightlifting session, and rose in muscle injury with no liver disease.
The numbers and sources
- Compared with
- The same men's results before exercise, and the laboratory's upper reference limit
- Effect
- After a single 1-hour weightlifting session in healthy men unused to lifting, ALT rose significantly and was still raised 7 days later. The highest value was 4.1 µkat/L against an upper reference limit of 0.7 µkat/L, and the median time to peak was 120 hours. At the follow-up visit 10 to 12 days after exercise, mean ALT was higher than mean AST [20]. In 16 patients with muscle necrosis from extreme exercise, polymyositis or seizures and no evidence of liver disease, ALT and AST were both elevated alongside markedly raised creatine kinase [21].
- Population
- 15 healthy men, mean age 24.5, 14 analyzed [20]. 16 patients with muscle injury [21].
- Sources
- [20], [21]
- Caveats
- Both studies are small. The exercise study used men not accustomed to weightlifting, and people who train regularly may respond differently [20]. The muscle injury study also reports the ratio of AST to ALT, a separate quantity not placed on this page [21].
What studies tie it to
Linked in research2
Death from liver disease
Linked to more deaths from liver disease, with risk rising from values of 20 U/L upward in one large Korean cohort.
The numbers and sources
- Effect
- In 142,055 Korean adults followed for 8 years, death from liver disease rose with ALT even inside the usual reference range. Compared with ALT below 20 IU/L, the adjusted relative risk in men was 2.9 (95% CI 2.4 to 3.5) at 20 to 29 IU/L and 9.5 (7.9 to 11.5) at 30 to 39 IU/L. In women it was 3.8 (1.9 to 7.7) and 6.6 (1.5 to 25.6). The cut-off that predicted liver disease in men with the greatest accuracy was 30 IU/L [10]. In 14,950 US adults without viral hepatitis followed for 12 years, ALT above 30 U/L in men or 19 U/L in women went with more deaths from liver disease (HR 8.2, 95% CI 2.1 to 31.9) [11].
- Population
- 94,533 men and 47,522 women aged 35 to 59 in the Korea Medical Insurance Corporation study [10]. 14,950 adults in the third US National Health and Nutrition Examination Survey, negative for hepatitis B and C markers [11].
- Sources
- [10], [11]
- Caveats
- Observational. Deaths were taken from death certificates. Liver disease deaths were 0.13% of the US cohort over 12 years, so the interval around that estimate is wide [11]. The authors of a US study note that results from South Korea would not necessarily apply to countries where different causes of liver disease predominate [6].
Type 2 diabetes
Linked to more type 2 diabetes, 16% higher risk per 5 U/L in pooled cohorts, a result the authors said publication bias may explain.
The numbers and sources
- Effect
- In a meta-analysis of 17 prospective studies, the relative risk of type 2 diabetes was 1.16 (95% CI 1.08 to 1.25) per 5 IU/L higher ALT and 1.26 (1.14 to 1.41) per standard deviation of log ALT, with high heterogeneity (I2 88%). The association became nonsignificant after correction for publication bias [12]. In a Mendelian randomization study, genetically predicted higher ALT was related to more type 2 diabetes (odds ratio 1.45 per standard unit, 95% CI 1.10 to 1.92) [13].
- Population
- 60,359 participants and 3,890 new cases of type 2 diabetes in 17 studies [12]. Up to 64,094 people with type 2 diabetes and 607,012 controls in the genetic study [13].
- Sources
- [12], [13]
- Caveats
- The cohort studies are observational and their pooled result did not survive correction for publication bias [12]. The genetic study's authors read their findings as support for insulin resistance leading to fatty liver, which in turn raises diabetes risk, so ALT may mark that process and not drive it [13].
Mixed results1
Death from any cause
Mixed results: pooled cohorts found fewer deaths at higher ALT in North America and more in Asia, and a US survey found no association.
The numbers and sources
- Effect
- In a meta-analysis of 19 cohort studies, comparing the top and bottom thirds of baseline ALT gave a relative risk of death from any cause of 0.82 (95% CI 0.78 to 0.86) in North American populations and 1.43 (1.08 to 1.90) in Asian populations [14]. In US adults without viral hepatitis, ALT above 30 U/L in men or 19 U/L in women was not associated with death from any cause (HR 1.2, 95% CI 0.88 to 1.6) [11].
- Population
- Over 9.24 million participants and 242,953 deaths in 19 cohorts, which also covered other liver enzymes [14]. 14,950 US adults followed for 12 years [11].
- Sources
- [14], [11]
- Caveats
- Observational. The authors of the meta-analysis could not explain the difference between regions and called for further study [14]. These studies cannot say why a higher ALT went with fewer deaths in the North American cohorts.
Checked, no link found1
Heart disease and stroke
Not linked to cardiovascular disease overall in a meta-analysis of 29 cohorts, with a slightly lower rate of coronary heart disease and a slightly higher rate of stroke.
The numbers and sources
- Effect
- A meta-analysis of 29 prospective cohorts found no evidence of an association of ALT with cardiovascular disease. In stratified analyses ALT was somewhat inversely associated with coronary heart disease (relative risk 0.95, 95% CI 0.90 to 1.00) and positively associated with stroke (1.01, 1.00 to 1.02) [15]. In US adults, ALT above 30 U/L in men or 19 U/L in women was not associated with cardiovascular death (HR 0.90, 95% CI 0.56 to 1.4) [11].
- Population
- Over 1.23 million participants and 20,406 cardiovascular outcomes in 29 cohorts, which also covered other liver enzymes [15]. 14,950 US adults [11].
- Sources
- [15], [11]
- Caveats
- Observational. The authors asked for more study of the opposite directions seen for coronary heart disease and stroke [15].
Sources
- US Food and Drug Administration. 21 CFR 862.1030, Alanine amino transferase (ALT/SGPT) test system. Electronic Code of Federal Regulations. https://www.ecfr.gov/current/title-21/section-862.1030
- Centers for Disease Control and Prevention, National Center for Health Statistics. National Health and Nutrition Examination Survey 2017-2018 Laboratory Procedure Manual: Alanine Aminotransferase (ALT), serum, Roche Cobas 6000. Performed by the University of Minnesota Advanced Research and Diagnostic Laboratory. https://wwwn.cdc.gov/nchs/data/nhanes/public/2017/labmethods/BIOPRO-J-MET-ALT-508.pdf
- Kwo PY, Cohen SM, Lim JK. ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries. American Journal of Gastroenterology. 2017. https://doi.org/10.1038/ajg.2016.517
- Terrault NA, Lok ASF, McMahon BJ, et al. Update on prevention, diagnosis, and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance. Hepatology. 2018. https://doi.org/10.1002/hep.29800
- Prati D, Taioli E, Zanella A, et al. Updated Definitions of Healthy Ranges for Serum Alanine Aminotransferase Levels. Annals of Internal Medicine. 2002. https://doi.org/10.7326/0003-4819-137-1-200207020-00006
- Ruhl CE, Everhart JE. Upper Limits of Normal for Alanine Aminotransferase Activity in the United States Population. Hepatology. 2012. https://doi.org/10.1002/hep.24725
- Lee JK, Shim JH, Lee HC, et al. Estimation of the Healthy Upper Limits for Serum Alanine Aminotransferase in Asian Populations With Normal Liver Histology. Hepatology. 2010. https://doi.org/10.1002/hep.23505
- Ceriotti F, Henny J, Queraltó J, et al. Common reference intervals for aspartate aminotransferase (AST), alanine aminotransferase (ALT) and γ-glutamyl transferase (GGT) in serum: results from an IFCC multicenter study. Clinical Chemistry and Laboratory Medicine. 2010. https://doi.org/10.1515/cclm.2010.315
- American Board of Internal Medicine. ABIM Laboratory Test Reference Ranges, January 2026. https://www.abim.org/Media/bfijryql/laboratory-reference-ranges.pdf
- Kim HC, Nam CM, Jee SH, et al. Normal serum aminotransferase concentration and risk of mortality from liver diseases: prospective cohort study. BMJ. 2004. https://doi.org/10.1136/bmj.38050.593634.63
- Ruhl CE, Everhart JE. Elevated Serum Alanine Aminotransferase and γ-Glutamyltransferase and Mortality in the United States Population. Gastroenterology. 2009. https://doi.org/10.1053/j.gastro.2008.10.052
- Kunutsor SK, Apekey TA, Walley J. Liver Aminotransferases and Risk of Incident Type 2 Diabetes: A Systematic Review and Meta-Analysis. American Journal of Epidemiology. 2013. https://doi.org/10.1093/aje/kws469
- De Silva NMG, Borges MC, Hingorani AD, et al. Liver Function and Risk of Type 2 Diabetes: Bidirectional Mendelian Randomization Study. Diabetes. 2019. https://doi.org/10.2337/db18-1048
- Kunutsor SK, Apekey TA, Seddoh D, Walley J. Liver enzymes and risk of all-cause mortality in general populations: a systematic review and meta-analysis. International Journal of Epidemiology. 2014. https://doi.org/10.1093/ije/dyt192
- Kunutsor SK, Apekey TA, Khan H. Liver enzymes and risk of cardiovascular disease in the general population: A meta-analysis of prospective cohort studies. Atherosclerosis. 2014. https://doi.org/10.1016/j.atherosclerosis.2014.06.006
- Ma X, Liu S, Zhang J, et al. Proportion of NAFLD patients with normal ALT value in overall NAFLD patients: a systematic review and meta-analysis. BMC Gastroenterology. 2020. https://doi.org/10.1186/s12876-020-1165-z
- Lazo M, Selvin E, Clark JM. Brief Communication: Clinical Implications of Short-Term Variability in Liver Function Test Results. Annals of Internal Medicine. 2008. https://doi.org/10.7326/0003-4819-148-5-200803040-00005
- Carobene A, Røraas T, Sølvik UØ, et al. Biological Variation Estimates Obtained from 91 Healthy Study Participants for 9 Enzymes in Serum. Clinical Chemistry. 2017. https://doi.org/10.1373/clinchem.2016.269811
- Dutta A, Saha C, Johnson CS, Chalasani N. Variability in the upper limit of normal for serum alanine aminotransferase levels: a statewide study. Hepatology. 2009. https://doi.org/10.1002/hep.23200
- Pettersson J, Hindorf U, Persson P, et al. Muscular exercise can cause highly pathological liver function tests in healthy men. British Journal of Clinical Pharmacology. 2008. https://doi.org/10.1111/j.1365-2125.2007.03001.x
- Nathwani RA, Pais S, Reynolds TB, Kaplowitz N. Serum alanine aminotransferase in skeletal muscle diseases. Hepatology. 2005. https://doi.org/10.1002/hep.20548