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Blood alanine aminotransferase levels >1,000 IU/l – causes and outcomes

Clin Med (Lond). 2015 Jun; 15(3): 244–247.

, specialist registrar gastroenterology,A, senior house officer,B, specialist registrar gastroenterology,C and , director and consultant gastroenterologistD

Zita Galvin

ACentre for Liver Diseases, Mater Misericordiae University Hospital, Dublin, Ireland

Anna McDonough

BCentre for Liver Diseases, Mater Misericordiae University Hospital, Dublin, Ireland

John Ryan

CCentre for Liver Diseases, Mater Misericordiae University Hospital, Dublin, Ireland

Stephen Stewart

DMater Misericordiae University Hospital, Dublin, Ireland

ACentre for Liver Diseases, Mater Misericordiae University Hospital, Dublin, Ireland

BCentre for Liver Diseases, Mater Misericordiae University Hospital, Dublin, Ireland

CCentre for Liver Diseases, Mater Misericordiae University Hospital, Dublin, Ireland

DMater Misericordiae University Hospital, Dublin, Ireland

Corresponding author. Address for correspondence: Dr Z Galvin, Centre for Liver Diseases, Mater Misericordiae University Hospital, 55 Eccles Street, Dublin 7, Ireland. Email: [email protected] © Royal College of Physicians 2015. All rights reserved.This article has been cited by other articles in PMC.

ABSTRACT

Standard medical education dictates that the vast majority of cases of an alanine aminotransferase (ALT) level >1,000 IU/l will be due to acute ischaemia, acute drug-induced liver injury (DILI) (usually paracetamol) or acute viral hepatitis. There are very few references in the literature to other potential causes of an ALT >1,000 IU/l nor to the prognosis ascribed to each aetiology. In this study, we have confirmed that the main causes of a dramatic ALT rise are ischaemic liver injury, DILI and viral hepatitis. Common bile duct stones and hepatitis E are two causes for which there needs to be a high index of suspicion as the necessary tests may not be in the clinician’s first-line investigation panel. Failing to find a cause and determining that the cause was ischaemic both have poor prognostic implications.

KEYWORDS : Alanine aminotransferase, transaminases, acute hepatitis, aetiology, prognosis

Introduction

Alanine aminotransferase (ALT) is an enzyme involved in the alanine cycle and is primarily found in muscle and the liver.1 In clinical practice, ALT is measured as one of the liver function tests (LFTs) to screen for hepatocellular injury.2 The differential diagnosis for elevated serum aminotransferases is broad and includes metabolic liver disease, alcohol-related liver disease, ischaemic hepatopathy, hepatotoxicity from drugs or toxins, autoimmune, hepatocellular and biliary injury, chronic viral hepatitis and malignant infiltration. Typically, ALT levels in these conditions can be two-to-five times the upper limit of normal, which is around 40 IU/l in most hospitals. Occasionally ALT levels can rise to levels of >1,000 IU/l. This will usually lead to an urgent referral to hospital or within hospital to the gastroenterology or hepatology teams. Standard medical education dictates that the vast majority of these cases will be due to acute ischaemia or congestion, acute drug-induced liver injury (DILI) (usually paracetamol) or acute viral hepatitis.3–5 The requirement for admission to hospital and the prognostic and treatment implication for these three groups of conditions are very different and as such, it is important to determine the cause of the dramatic ALT elevation early.

Our aim was to review all the cases with an ALT level >1,000 IU/l in our city centre university hospital in order to determine cause and prognosis and improve urgent care pathways.

Materials and methods

This single-centre, retrospective, observational study was conducted in a tertiary referral university hospital over a two-year period. A retrospective chart review was performed on every patient who had presented to the hospital over this time period with an ALT >1,000 IU/l. This included reviewing, where applicable, the primary care referral letters for that episode, the written and electronic patient charts, patient medication records, intensive care unit (ICU) discharge summaries, hospital discharge summaries and death notifications. Where possible, aetiology was ascribed and prognosis (survival to hospital discharge) was recorded. In all cases, the aetiology ascribed in the patient notes was correlated with diagnostic criteria that had been established prior to the review (Table ). All data were anonymised and recorded in a secure dedicated electronic database. Statistical data analysis was carried out using SPSS version 20. The study protocol was approved by the Research Ethics Committee of the Mater Misericordiae University Hospital (MMUH 1/378/1545 TMR).

Table 1. 

Diagnostic features of acute liver injury (ALT >1,000 IU/l).

Results

In total, 182 patients (56% (n = 102) male and 44% (n = 80) female) with an ALT >1,000 IU/l were identified.

The aetiology of the raised ALT is shown in Fig . As expected, ischaemic liver injury (61%, n = 111), DILI (15.9%, n = 29) and acute viral hepatitis (12.1%, n = 22) were the most common causes accounting for nearly 90% of all cases. Interestingly, the next most common causes were idiopathic (5.0%, n = 9) and acute choledocholithiasis (4.4%, n = 8). Autoimmune hepatitis (1.6%, n = 3) made up the remaining cases.

Aetiology of liver injury in patients with an ALT >1,000 IU/l (%) (n = 182). ALT = alanine aminotransferase.

Paracetamol toxicity accounted for almost half (13/29) of the DILI cases. The other common causes were anti-tuberculosis medications (6/29) and other antibiotics (4/29). Other drugs were also implicated in smaller numbers (Table ).

Table 2. 

DILI causes of an ALT >1,000 IU/l (n = 29).

In order of frequency, the viral hepatitides causing ALT >1,000 IU/l were hepatitis B (7/22), hepatitis C (5/22), hepatitis E (4/22) and hepatitis A (3/22). Cytomegalovirus, Epstein–Barr virus and varicella zoster each accounted for one case.

9.3% (n = 17) of patients had their acute hepatitis managed as outpatients, 54.9% (n = 100) were admitted to the hospital and discharged home well and 35.7% (n = 65) died during their admission (Fig ). Survival was highly dependent on the aetiology of the raised ALT. Ischaemic liver injury was the cause of the ALT >1,000 IU/l in the vast majority of patients who died during the admission (93.8%, n = 61) (Fig ). Overall mortality was 55% (61/111) in the ischaemic group, 6.9% (2/29) in DILI and 0% if the aetiology was viral hepatitis, stone disease or autoimmune hepatitis. 22.2% (2/9) of those patients in whom a cause could not be identified died.

(A) Outcome of patients who presented with an ALT >1,000 IU/l (%) (n = 182). (B) Aetiology of ALT >1,000 IU/l in the deceased cohort (%) (n = 65; 35.7% of total cohort). ALT = alanine aminotransferase; DILI = drug-induced liver injury.

Conclusions

We reviewed the investigations and outcomes of 182 cases where the ALT measurement was >1,000 IU/l. The results were generated by the biochemistry department attached to a tertiary referral university hospital and could come from the hospital in-patients or patients attending local general practitioners. The vast majority of these patients were admitted to hospital but some were managed in the community by primary care or in the hepatology out-patient department. There were some findings that reinforced standard teaching around ‘acute hepatitis’ and some that were surprising.

To the best of the authors knowledge, no similar case series has been published, however, a review of the literature reveals that ischaemia, drugs and toxins can cause elevations in ALT of greater than 40 times the upper limit of normal (ULN) while viral aetiology generally causes elevations of 10 to 40 times the ULN, ie any of these aetiologies can cause an ALT of >1,000 IU/l.7,8 Prognosis largely depends on aetiology and as such it is important to make the correct diagnosis from the outset. There are no specific blood tests for ischaemic or DILI and so detailed history taking and a thorough physical examination are essential in order to make the correct diagnosis. A number of laboratory tests and patterns may also be useful. In viral hepatitis, transaminases rarely increase to greater than 40 times ULN unlike that seen in ischaemic or DILI. Lactate dehydrogenase (LDH) activity often is higher than that of AST at presentation in ischaemic or drug-induced hepatic injury,8,9 as compared with viral hepatitis when the LDH level is generally normal or only slightly above the ULN.10 Choledocholithiasis is a recognised but rare cause of severe transaminitis.11 Agahi et al described three cases of choledocholithiasis causing an ALT >1,000 IU/l, all of these cases had repeated investigation for liver disease before eventual identification of common bile duct stones with magnetic resonance cholangiopancreatogram.12 Presentation of fulminant AIH has been described with transaminases of >1,000 IU/l, but it is rare. 13 A recent single-centre review of all cases of AIH over a ten-year period identified 32 cases of acute severe AIH (defined as an international normalised ratio >1.5 without evidence of fibrosis). Although exact numbers were not given, the average AST was 619 IU/l (116–2,690 IU/l) indicating that very few patients had an AST of >1,000 IU/l.14

The proportion of patients that had ischaemic injury, DILI or viral hepatitis was exactly as we would have expected at around 90%. We were surprised to find choledocholithiasis as the next most common cause of an ALT >1,000 IU/l (8/182 cases). This is significantly higher than the incidence rates seen in the literature and may confound admitting teams who would expect biliary colic due to bile duct obstruction to present with obstructive LFTs.

The second important clinically relevant finding from this study was that hepatitis E was more frequently detected than hepatitis A. This was in spite of hepatitis A serology being in the first-line viral screen and the need for hepatitis E serology to be requested separately if the first-line screen is negative. Hepatitis E is one of the most common causes of acute hepatitis worldwide, with the majority of cases occurring in Asia. In recent years, however, an increasing number of acute and chronic hepatitis E virus infections have been reported in industrialised countries.15 This has both clinical and treatment implications. In the first instance, a positive viral serology test allows the clinician to stop searching for other causes and may avoid liver biopsy. In addition, hepatitis E infection can become chronic in immunocompromised patients and lead to hepatic fibrosis and cirrhosis. Treatment strategies are currently being evaluated and attempts are being made to develop effective hepatitis E virus vaccines.16 Physicians need to be aware of hepatitis E as a cause of both acute and chronic hepatitis in immunocompromised patients and this is particularly important if there may be a risk of pregnant women being exposed to infection given the high maternal mortality associated with the syndrome.

Nine patients had no cause identified for their acute transaminases. Four of these patients were not admitted to our institution nor were they referred to hepatology outpatient clinics. It was established that these patients were still alive but it was not possible to retrospectively establish the cause of the liver injury. They may have been referred to another local hospital or managed in the community. Despite extensively reviewing the clinical notes for the remaining five patients, it was not possible to confidently attribute a cause for the liver injury. There were no recorded hypotensive episodes, viral serology was negative and no incriminating drugs were recorded in the medical history. It is important to highlight that none of the patients were checked for hepatitis E. A retrospective effort to establish the hepatitis E virus status of these patients was not successful because samples were no longer available (stored for six months).

Finally, the clinical courses are very different for each of the aetiologies of liver injury. This has implications for follow-up. The prognosis in acute viral hepatitis, even with ALT >1,000 IU/l is extremely good and these patients can almost always be managed closely in the community. DILI has a well-defined mortality which will be drug-dependent and, certainly in the case of paracetamol, very predictable. Patients in whom the ALT rises to >1,000 IU/l due to ischaemic liver injury have a very poor prognosis. Often this is evident at the time, with the liver being simply another organ insulted in multi-organ failure. Sometimes, however, the ALT rise may be one of the earlier signs that augurs poorly for patient prognosis.

Limitations of this study are similar to those seen in other retrospective studies. This study depended on the availability, accuracy and comprehensiveness of the medical records. In the majority of cases it was possible to confidently attribute an aetiology to each patient; however there were a small number of cases where an educated assumption needed to be made. It was not possible to retrospectively apply diagnostic criteria such as the CIOMS/RUCAM scale for DILI,17 to check LDH, or to complete the viral or autoimmune screens in those who had some missing results. There were nine cases where it was not possible to define an aetiology. The high mortality seen in the idiopathic group could possibly be explained by the fact that some of this group were in fact unrecognised ischaemic or drug-induced injuries.

In summary we have defined the main causes of a dramatic ALT rise and associated a prognosis with each aetiological group. Common bile duct gallstones and hepatitis E are two causes for which there needs to be a high index of suspicion, as the necessary tests may not be in the first-line investigation panel of the clinician. Failing to find a cause and determining that the cause was ischaemic both have poor prognostic implications.

References

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Alanine transaminase (ALT) blood test

Definition

The alanine transaminase (ALT) blood test measures the level of the enzyme ALT in the blood.

Alternative Names

SGPT; Serum glutamate pyruvate transaminase; Alanine transaminase; Alanine aminotransferase

How the Test is Performed

A blood sample is needed.

How to Prepare for the Test

How the Test will Feel

When the needle is inserted to draw blood, some people feel moderate pain. Others feel only a prick or stinging. Afterward, there may be some throbbing or a slight bruise. This soon goes away.

Why the Test is Performed

ALT is an enzyme found in a high level in the liver. An enzyme is a protein that causes a specific chemical change in the body.

Injury to the liver results in release of ALT into the blood.

This test is mainly done along with other tests (such as AST, ALP, and bilirubin) to diagnose and monitor liver disease.

Normal Results

The normal range is 4 to 36 U/L.

Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or may test different samples. Talk to your health care provider about the meaning of your specific test results.

What Abnormal Results Mean

An increased ALT level is often a sign of liver disease. Liver disease is even more likely when the levels of substances checked by other liver blood tests have also increased.

An increased ALT level may be due to any of the following:

  • Scarring of the liver (cirrhosis)
  • Death of liver tissue
  • Swollen and inflamed liver (hepatitis)
  • Too much iron in the body (hemochromatosis)
  • Too much fat in the liver (fatty liver)
  • Lack of blood flow to the liver (liver ischemia)
  • Liver tumor or cancer
  • Use of drugs that are toxic to the liver
  • Mononucleosis (“mono”)
  • Swollen and inflamed pancreas (pancreatitis)

Risks

There is little risk involved with having your blood taken. Veins and arteries vary in size from one person to another and from one side of the body to the other. Taking blood from some people may be more difficult than from others.

Other risks associated with having blood drawn are slight, but may include:

  • Excessive bleeding
  • Fainting or feeling lightheaded
  • Multiple punctures to locate veins
  • Hematoma (blood collecting under the skin)
  • Infection (a slight risk any time the skin is broken)

References

Chernecky CC, Berger BJ. Alanine aminotransferase (ALT, alanine transaminase, SGPT) – serum. In: Chernecky CC, Berger BJ, eds. Laboratory Tests and Diagnostic Procedures. 6th ed. St Louis, MO: Elsevier Saunders; 2013:109-110.

Pincus MR, Tierno PM, Gleeson E, Bowne WB, Bluth MH. Evaluation of liver function. In: McPherson RA, Pincus MR, eds. Henry’s Clinical Diagnosis and Management by Laboratory Methods. 23rd ed. St Louis, MO: Elsevier; 2017:chap 21.

Pratt DS. Liver chemistry and function tests. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 10th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 73.

Alanine Aminotransferase – an overview

A Alanine Aminotransferase

Alanine aminotransferase (EC 2.6.1.2) (ALT), formerly known as glutamic pyruvate transaminase, catalyzes the reversible transamination of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. ALT, along with other transaminases, plays a role in amino acid catabolism and interorgan nitrogen transport. Pyridoxal 5′-phosphate (PP) is the cofactor of ALT, thus forming the active holoenzyme. PP is generally present in serum in sufficient quantities to provide near maximum activity of the ALT with only a reported 11% and 7% inactive apoenzyme in dog and cat serum, respectively (Stokol and Erb, 1998). There was no difference found between the percentage of inactive apoenzyme in the serum of normal animals and those with hepatic disease. However, two dogs were identified with 14,225% and 336% greater serum ALT activity when PP was added (Mesher et al., 1998). Approximately half the ALT in serum from a group of exercising Thoroughbred horses was in the inactive apoenzyme form (Rej et al., 1990). Hence, because there are cases in which PP seems to be limiting the measured ALT activity, some, but not all, commercial assays for ALT now contain added PP reagent.

ALT activity is found in several body organs, but the magnitude of activity varies dramatically with species. In dogs, the ALT activity per gram of liver is at least four times greater than in other organs, although considerable activity is found in both heart and skeletal muscle (Clampitt and Hart, 1978; Keller, 1981; Zinkl et al., 1971). Similar findings are true for cats, but in horses, cattle, and swine, the ALT activity per gram of tissue differs little in liver when compared to muscle. Hence, based on tissue concentrations of ALT, increased serum ALT activity is somewhat specific for hepatic injury in dogs and cats but offers no specificity for detection of liver injury in horses and cattle.

ALT, found in the cytoplasm of hepatocytes, is also found in mitochondria but generally at considerably lower concentrations, depending on species and tissue. Although it has been suggested that the mitochondrial enzyme may be released into blood more slowly following hepatocellular injury, this activity is still poorly understood and has not been utilized as a diagnostic tool.

The half-life of ALT in blood is not clearly defined, although the circulation time is obviously adequately long to evaluate organ injury and release of ALT into blood for hours to days after the event. In dogs, reports have suggested half-lives of 3, 20, 45, and 60 h (Fleisher and Wakim, 1963; Reichard, 1959; Zinkl et al., 1971). Semilogarithmic plots of the decline in serum ALT activity following peak activity induced by acute CCl4 exposure suggest a half-life of between 45 and 60 h in dogs, although this may be a slight overestimation, as injured tissue is still likely present and contributing to the blood pool (unpublished data). The half-life of ALT from feline liver extracts, administered intravenously to cats, was estimated as 3 to 4 h (Nilkumuhaug and Thornton, 1979). This is consistent with the half-life of 6 h for ALP activity in the blood of cats (Hoffman et al., 1977).

Serum ALT has been recognized as a marker of hepatocellular injury since the 1950s (Chimsky et al., 1956; Cornelius, 1958). The use of ALT as a diagnostic tool was expedited by the development in the mid-1950s of a simple coupled assay for ALT activity in serum that eliminated the problem of product inhibition (Reitman and Frankel, 1957). Numerous studies using carbon tetrachloride have clearly shown the value of serum ALT as an indicator of hepatocellular necrosis, especially in dogs and cats, but to a much lesser extent in horses, cattle, swine, sheep, and goats (Cornelius et al., 1958; Everett et al., 1977; Noonan, 1981; Noonan and Meyer, 1979; Spano et al., 1983; Turgut et al., 1997; Zinkl et al., 1971). The length of time that serum ALT activity is increased ranges from 9 to 23 days in dogs, which suggests prolonged injury to the liver but also supports the longer half-life suggested earlier (Guelfi et al., 1982; Noonan, 1981; Turgut et al., 1997). Relatively mild increases in serum ALT activity occur in dogs and cats with biliary obstructive diseases that cause serum ALP activity to increase markedly (Everett et al., 1977; Spano et al., 1983). Hence, the ratio of serum ALT-to-ALP activity is far greater in cases of hepatic necrosis than with cholestasis, suggesting that very general interpretive conclusions can be made by comparing the magnitude of increase of serum activity of these two enzymes. Increased serum ALT activity occurs with a wide range of other disorders including hypoxia secondary to anemia, metabolic diseases such as lipidosis, nutritional disorders such as copper toxicosis, inflammatory or infectious diseases, neoplastic diseases, and traumatic liver injury. Increased serum ALT activity has also been associated with numerous drugs; in many cases, these are likely idiosyncratic reactions causing hepatocellular toxicity. Exposure to carbon tetrachloride, mushroom alkaloids, or acetaminophen is clearly a hepatotoxic event.

Mild to moderate increases in serum ALT activity are also observed in dogs and cats with endocrine diseases such as diabetes mellitus, hyperthyroidism, hyperadrenocorticism, and hypothyroidism. For example, 163 (78%) dogs with diabetes mellitus have increased serum ALT activity (Hess et al., 2000). Cats with diabetic ketoacidosis commonly have increased serum ALT activity (Bruskiewicz et al., 1997). Increased serum ALT activity is common in dogs with hyperadrenocorticism or dogs treated with glucocorticoids (DeNova and Prasse, 1983; Dillon et al., 1980; Solter et al., 1994). It has been shown in rats that ALT synthesis may be induced by glucocorticoids in order to increase function of the gluconeogenic pathways. However, experimental treatment of healthy dogs with glucocorticoids did not result in an increase in the concentration of hepatic tissue ALT activity, suggesting that increased hepatic mass plays a larger role than increased hepatocellular enzyme induction for an observed increased serum ALT activity (Solter et al., 1994).

Although early studies of increased serum ALT activity following experimentally induced hepatocellular injury and the studies demonstrating much higher ALT activity in liver than other organs led to the early conclusion that increases of ALT activity in serum are specific for hepatocellular injury, there is clear evidence that serum ALT activity can also be increased as a result of injury to myocytes as well. Dogs in a colony with canine X-linked muscular dystrophy and ongoing muscle necrosis had increased serum CK, AST, and up to a 25-fold increase in ALT activity but a normal SDH activity, suggesting that myonecrosis contributed to the increased serum ALT activity (Valentine et al., 1988). This is consistent with the presence of some ALT activity in cardiac and skeletal muscle of dogs. In a case report of a cat with myokymia and neuromyotonia, the CK activity was 28,380, whereas the ALT activity was only 195 U/l; in a study of rhabdomyolysis in three dystrophin-deficient cats, the CK activity ranged up to 2040 times the upper limit of the reference range, whereas the ALT activity only increased to 19 times the upper limit of the reference range, suggesting only a minimal increase of serum ALT activity should be expected with muscle injury in this species (Galano et al., 2005; Gaschen et al., 1998).

Although at least one early study in dogs showed a correlation between the magnitude of serum ALT activity and histological evidence of necrosis, other studies have reported little correlation (VanVleet and Albert, 1968). Similarly, bile duct ligation of dogs led to a 25-fold increase in serum ALT activity with minimal evidence of hepatocellular necrosis. As discussed in the introduction, the recognition of the formation of membrane blebs on hepatocytes and the rupture of these blebs during various conditions such as endotoxic shock, carbon tetrachloride-induced injury, cholestasis, and experimentally induced hypoxia have led to the understanding that there can be an increase of serum enzymes derived from the cytoplasm of the cell in cases of reversible cellular injury. In summary, the observation of increased serum ALT activity indicates hepatocellular (or myocyte) injury, but it does not necessarily imply irreversible injury and does not suggest a specific cause.

ALT – eClinpath

Synonyms

Glutamate pyruvate transaminase (GPT)

Physiology

Alanine aminotransferase (ALT) catalyzes the transfer of the alpha amino group of alanine to alpha-ketoglutaric acid, resulting in the formation of pyruvic and glutamic acid. ALT is mostly located in the cytoplasm (with small amounts in mitochondria) and like AST, requires cofactor P5P for maximal enzyme activity.

It is useful as a specific indicator of hepatocellular injury in dogs and cats. ALT is not a useful indicator of liver disease in large animals, and pigs, due to low enzyme activity in liver tissue of these species. SDH and GLDH are viable alternatives to ALT in all species.

Serum half-life is 59 hours in dogs and < 24 hours (about 3-4 hours) in cats. Following acute hepatic injury, serum enzyme activity peaks at about 48 hours and then begins to decrease. Increases in the enzyme occur due to cell damage (increased membrane permeability, blebbing or necrosis), which may be transient or permanent (reversible or irreversible).

Organ specificity

ALT is found in the liver, muscle (cardiac and skeletal), kidneys, and erythocytes (in some species). ALT is fairly liver specific in dogs, cats, rabbits, rats and primates. Some increases are possible in severe muscle diseases of the dog and cat due to release of enzyme from this tissue (in this situation, higher increases in AST are typically seen).

Method


The following colorimetric method is used at Cornell University:

Reaction type

Kinetic

Procedure

This two step process commences with ALT catalyzing the reaction between α-ketoglutarate and L-alanine to form L-glutamate and pyruvate. ALT catalyzes this reaction to equilibrium and the increased levels of pyruvate are quantified by its subsequent reduction by NADH in the presence of lactate dehydrogenase (LDH). Decreased levels of NADH are measured photometrically and are proportional to the rate of formation of pyruvate, which correlates to ALT activity. Reaction is shown below:

L-alanine + α-ketoglutarate     ALT      > pyruvate + L-glutamate

Pyruvate + NADH + H+   LDH    > L-lactate + NAD+

Units of measurement

Enzyme activity is measured in U/L (U = international unit) and µkat/L (SI units), which is defined as the amount of enzyme that catalyzes the conversion of 1 µmol of substrate per minute under specified conditions. The conversion formula is shown below:

U/L x 0.0167 = µkat/L

Sample considerations


Sample type

Serum and plasma

Anticoagulant

Heparin, EDTA

Stability

The stability of ALT activity in human serum and plasma samples is as follows (per product information sheet): 3 days at 15-25 °C, 7 days at 2 – 8 °C, and more than 7 days at (-60)-(-80) °C.

Interferences

  • Lipemia/Turbidity, icterus: No significant interferences.
  • Hemolysis: In some species, such as cats and pigs, intravascular or in vitro hemolysis may increase activity due to the ALT release from erythrocytes. In pigs, hemolysis of >100 units increased ALT by a median of 8 U/L (di Martino et al 2015).
  • Drugs: Anticonvulsants (primidone, phenobarbitone, dilantin) can increase ALT activity up to 4 x normal. Although these drugs were thought to induce ALT synthesis, increases in ALT activity are mostly thought to be secondary to hepatocellular necrosis. Corticosteroids increase ALT to approximately 2-3 x normal. Activity is higher in dogs with steroid hepatopathy (where actual hepatocellular injury occurs). This is currently attributed to altered permeability and not due to increased synthesis. Any drugs that can cause hepatotoxicity can result in increased ALT activity, e.g. tetracycline in cats, caparsolate in dogs, acetaminophen. Certain drugs may decrease ALT (and AST) activity, by impairing activation of vitamin B6 to P5P, e.g. cephalosporin, cyclosporin, isoniazide.

Test interpretation


Increased ALT activity


As a guideline to degree of increase, a 2-3 fold increase (compared to the upper reference limit) is mild, 4-5 fold increase is moderate, and >10 fold increase is marked. Degree of change is variable among clinicians and clinical pathologists.

  • Artifact: Intravascular or in vitro hemolysis may cause increased levels in the cat or pig. Cats have a high RBC to plasma ALT ratio. In contrast, hemolysis (intravascular or in vitro) has a minimal effect on ALT in cattle, horses, and dogs.
  • Pathophysiologic:
    • Liver disease: Increases in ALT activity can be seen with both primary and secondary hepatic disease, if altered cell membrane permeability or necrosis occur, and are not specific for the cause of hepatic disease.  Highest increases are seen in necrotizing or inflammatory conditions and some diseases, e.g. hepatocellular carcinoma or hepatic insufficiency, may not be associated with any increases in ALT if active hepatocyte injury is not occurring. Usually ALT activity exceeds AST activity in liver disease. Bile duct obstruction or other causes of cholestasis may increase ALT (and AST) activity due to the toxic effects of retained bile salts on hepatocytes. With cholestasis, the fold increases in cholestatic enzymes (ALP, GGT) and bilirubin are usually higher than the fold increases in liver leakage enzymes, which can help identify the primary pathologic process as cholestasis, which is then leading to liver injury. When liver injury causes cholestasis, the fold increases in leakage enzymes will be higher than that of the induction enzymes and total bilirubin may be normal or only mildly increased. Trauma will often increase ALT activity, even without morphologic evidence of cell injury.
    • Muscle disease: In large animals, ALT activity will increase with muscle injury and is not more useful than AST in this regard so it is not included on large animal chemistry panels. In small animals with severe muscle injury (ischemic myopathy in cats, muscular dystrophy in dogs, where CK activity is usually > 10,000 U/L), ALT will increase with CK and AST activities. However, the increases in ALT activity are usually less than increases in AST activity in primary muscle disease and SDH values should be normal (unless there is concurrent liver injury) (Valentine et al 1990).
    • Hyperthyroidism: Cats with hyperthyroidism often have mild increases in ALT, AST and ALP activities.

Assessment of the relationship of serum liver enzymes activity with general and abdominal obesity in an urban Bangladeshi population

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  • Smoking and Alanine Aminotransferase Levels in Hepatitis C Virus Infection: Implications for Prevention of Hepatitis C Virus Progression | Infectious Diseases | JAMA Internal Medicine

    Background 
    Alcohol consumption is a well-known risk factor for elevated ALT levels, but the role of cigarette smoking is unclear.

    Methods 
    We collected a cross-sectional sample of 6095 inhabitants 35 years or older in a community with hyperendemic hepatitis B and C virus infections. We assayed levels of serum alanine aminotransferase (ALT), hepatitis B surface antigen (HBsAg), and anti–hepatitis C virus antibody (anti-HCV). Multivariate logistic regression was performed to determine the factors for elevated ALT levels (≥40 U/L) among people with different hepatitis infection statuses.

    Results 
    Prevalence of elevated ALT levels in individuals who were seronegative for both infections or seropositive for HBsAg or anti-HCV was 3.9%, 11.1%, and 30.8%, respectively. Subjects with elevated ALT levels were more likely to be seropositive for anti-HCV, male, and seropositive for HBsAg; to drink alcohol; to smoke; and to have undergone blood transfusion (P<.05). An association was found between elevated ALT levels and the consumption of cigarettes and alcohol among anti-HCV–seropositive subjects. In multivariate logistic analyses, alcohol consumption (odds ratio [OR], 2.2; 95% confidence interval [CI], 1.2-4.1) and smoking (OR, 1.8; 95% CI, 1.1-2.7) were significantly associated with elevated ALT levels among anti-HCV–seropositive subjects, but no such association was found among HBsAg-seropositive subjects. The odds of elevated ALT levels were 7 times higher (95% CI, 2.7-18.8) for the anti-HCV–seropositive patients who smoked 1 or more packs of cigarettes per day and frequently drank alcohol than for those who did not.

    Conclusions 
    Smoking and alcohol consumption are independently associated with elevated ALT levels among anti-HCV–seropositive individuals but not among HBsAg-seropositive individuals. Patients who are seropositive for anti-HCV are strongly advised not to smoke and drink alcohol to reduce the possible risk for aggravating the liver dysfunction.

    SERUM ALANINE aminotransferase (ALT) is the most suitable and useful protein enzyme used in the evaluation of hepatocellular damage. It is also a surrogate marker for disease severity or index of hepatic activity.1,2 Elevated ALT levels are associated with obesity, sex, alcohol consumption, use of medication, and viral hepatitis infection.2-4 Its association with viral hepatitis infection makes the ALT level a useful indicator of drug efficacy in the treatment of hepatitis B (HBV) and C virus (HCV).5,6

    Alcohol consumption is a well-known risk factor for alcoholic liver diseases, cirrhosis, and hepatoma, independent of HBV or HCV infection.7,8 An additive or possibly synergistic effect exists between alcohol consumption and HCV on elevated ALT levels.9 However, the effect of smoking on the activity of serum ALT among patients with HBV or HCV infection has not been widely reported. Whether the effect is additive to that of alcohol consumption or depends on hepatitis infection status remains unclear.

    The aim of this study was to determine whether an association exists between alcohol consumption and ALT level, and between cigarette smoking and ALT level, and whether the relationships vary according to hepatitis infection status. These questions are important because, if these risk behaviors have different effects on ALT levels for different hepatitis infection statuses, they could provide evidence of different viral activity under the influence of alcohol consumption and/or cigarette smoking that could be helpful for secondary prevention. Previous studies of elevated ALT levels were mostly hospital based or conducted in regions with low prevalences of seropositivity for hepatitis B surface antigen (HBsAg) or anti-HCV antibody. To our knowledge, no large-scale population study on elevated ALT levels has been performed in a community with a high prevalence of HBsAg and anti-HCV seropositivity.10 We surveyed a community with hyperendemic HBV and HCV infection to determine the risk factors for elevated ALT levels.

    In A-Lein, a township of about 30 000 in southern Taiwan, patients with serious liver diseases abound, and mortality due to hepatoma is more than double the average in Taiwan,11 which exceeds 30 cases per 100 000 per year. This rate is at least 6 times higher than that of the countries in low-risk areas such as northern Europe and the United States.12 In a community-wide hepatitis screening of the 8800 adults 35 years or older in A-Lein, the prevalence of anti-HCV seropositivity was found to be approximately 17% and of HBsAg seropositivity to be approximately 13%.10 The study lasted from January 1, 1996, through December 31, 1997. Intensive health promotion activities for hepatitis screening were held before blood samples and questionnaires were collected. Villagers came voluntarily during this period. We have found no differences in the age, sex, health behaviors, or prevalence of HBV and HCV between the responders and nonresponders. A total of 6095 persons participated in this hepatitis screening program, a response rate of 69.3%.

    The questionnaire asked about demographic data, average daily consumption of cigarettes, the habit of alcohol consumption, and blood transfusions. The habit of drinking alcohol was subclassified as frequent, occasional, or rare. Cigarette consumption was defined as (1) equal to or greater than 1 pack per day (PPD), (2) less than 1 PPD, (3) abstained (stopped ≥6 months before this study), or (4) never smoked. The town had no reported cases of human immunodeficiency virus infection and was believed to have no or a negligible number of intravenous drug abusers among the target population. Very few people who were seropositive for HBsAg or anti-HCV had received interferon therapy.

    Serum samples were sent to the Tainan Blood Center of the Chinese Blood Service Foundation, Tainan, Taiwan, to test for HBsAg and anti-HCV markers and ALT levels. Seropositivity for HBsAg was determined by means of an enzyme immunoassay method (Version I; Murex, London, England). Seropositivity for anti-HCV was tested by means of the third-generation Murex anti-HCV enzyme immunoassay method, which contains the antigen from the HCV core and nonstructural 3, 4, and 5 regions. Levels of ALT were measured by means of a kinetic UV test for clinical chemistry analyzers (Olympus System Reagent; Olympus Diagnostica GmbH, Mills, Ireland). The cutoff value for diagnosis of elevated ALT level was set at 40 U/L according to the suggestion of the Blood Center of the Chinese Blood Service Foundation; this standard was also adopted by the National Health Insurance Bureau for eligibility of claims about liver disorders. The same cutoff value has been used for identifying communities with a high prevalence of HCV infection.13 In this study, HBsAg seropositivity also indicates anti-HCV seronegativity; anti-HCV seropositivity also indicates HBsAg seronegativity; and seronegativity describes the negative status for both infections.

    Univariate analysis and multiple logistic regression were used to determine the association of risk factors for elevated ALT levels (<40 vs ≥40 U/L). Multivariate logistic analysis was used to determine the risk factors for elevated ALT levels among seronegative, HBsAg-seropositive, and anti-HCV–seropositive individuals. The factors included in the multivariate logistic regression analysis were sex, stratified age (<40, 40-49, 50-59, and ≥60 years), alcohol and cigarette consumption, and blood transfusion. In multivariate logistic regression analysis, individuals with coinfection (HBsAg and anti-HCV seropositivity) were not included. We analyzed all results using Stata software.14

    Of the 6095 community members who participated in this study, 9.2% had elevated ALT levels (≥40 U/L). The prevalences of elevated ALT levels in individuals who were seronegative, seropositive for HBsAg, and seropositive for anti-HCV and coinfected were 3.9%, 11.1%, 30.8%, and 23.1%, respectively. Individuals who were seropositive for HBsAg were 3 times more likely to have elevated ALT levels than seronegative individuals (odds ratio [OR], 3.1; 95% confidence interval [CI], 2.3-4.1). Individuals who were seropositive for anti-HCV were 11 times more likely to have elevated ALT levels than seronegative individuals (OR, 11.0; 95% CI, 8.9-13.5). In addition, individuals who were male, habitual (frequent) drinkers of alcohol, or habitual smokers of cigarettes (≥1 PPD) or who had undergone a blood transfusion were more likely to have elevated serum ALT levels (P<.05) (Table 1). The mean and median levels of ALT in the various comparison groups are also shown in Table 1. Among these variables, anti-HCV–seropositive and coinfected individuals and those with frequent alcohol consumption had higher mean and median ALT levels.

    In multivariate logistic regression analysis of the risk factors for elevated ALT levels stratified by hepatitis infection status, no significant factor affected HBsAg-seropositive subjects, whereas alcohol consumption (OR, 2.2; 95% CI, 1.2-4.1) cigarette smoking (OR, 1.8; 95% CI, 1.1-2.7), and being aged 50 to 59 years (OR, 1.4; 95% CI, 1.0-2.0; P = .045) were significant factors associated with elevated ALT levels among anti-HCV–seropositive subjects (Table 2). Among seronegative subjects, being male (OR, 1.5; 95% CI, 1.0-2.2), drinking alcohol (OR, 2.7; 95% CI, 1.6-4.5), being aged 40 to 49 years (OR, 1.7; 95% CI, 1.2-2.5), and having undergone a blood transfusion (OR, 1.6; 95% CI, 1.0-2.4) were significant factors for elevated ALT levels, but those in older stratified age groups were less likely to have elevated ALT levels (OR, 0.98; 95% CI, 0.97-0.99).

    The additive effect of cigarette and alcohol consumption on elevated ALT levels was found among anti-HCV–seropositive subjects. The risk (70.0%) was highest among those who habitually smoked 1 PPD or more and who frequently drank alcohol (Figure 1). The odds of elevated ALT levels were 7 times higher (95% CI, 2.7-18.8) for that group than for those who did neither. An association between the prevalence of elevated ALT levels and the levels of alcohol drunk and cigarettes smoked was found in the anti-HCV–seropositive group but not in the HBsAg-seropositive group. Figure 1 also shows that the ALT level is more elevated for heavy smokers (≥1 PPD) than for frequent drinkers who did not smoke (50.0% vs 44.4%).

    This study demonstrates that consumption of cigarettes and alcohol are associated with elevated ALT levels among anti-HCV–seropositive subjects but not among HBsAg-seropositive subjects. Furthermore, cigarette smoking and alcohol consumption had an additive effect on the prevalence of elevated ALT levels in these patients. These results indicate that cigarette smoking and alcohol consumption are closely associated with the prevalence of elevated ALT levels in anti-HCV–seropositive individuals. The prevalence of elevated ALT levels for those who only smoked heavily (≥1 PPD) is not less than the prevalence for those who only drank frequently (50.0% vs 44.4%), which implies that smoking, like alcohol consumption, is an independent promoting factor for hepatic necroinflammation. A plausible explanation for the significant effect of cigarette smoking on hepatic necroinflammation is that the liver is a target organ for the chemicals in tobacco and alcohol. Patients who were seropositive for anti-HCV with elevated ALT levels require repeated hospital visits for biochemical tests, ultrasonography, and medical treatment, and hepatocellular carcinoma is more likely to develop than in those with normal ALT levels.15,16 Therefore, abstinence from smoking and alcohol consumption by anti-HCV–seropositive individuals could probably help to slow their progression into advanced liver diseases and minimize their need for health care services. At present, treatment for chronic HCV infection is recommended for patients with persistently elevated ALT levels,17 and no rationale exists for treating anti-HCV–seropositive patients with normal ALT levels.18 Patients who are seropositive for anti-HCV and who have active, heavy alcohol intake are not recommended for treatment, because alcohol increases viremia and interferes with the response to treatment.9 It is also rational to advise all anti-HCV–seropositive patients, particularly those with elevated ALT levels, to stop smoking to eliminate the additive effect that smoking has on HCV antibodies. Whether this will cause elevated ALT levels to return to normal in some patients needs further study. However, to suggest that they abstain from smoking before initiating expensive and unpleasant anti-HCV treatment might be a cost-effective measure and might increase treatment response.

    A high prevalence of HCV infection and rate of viral replication, rapid changes in histological progression of liver lesions, and increased carcinogenesis have been noted in patients with alcoholic liver diseases.8,9,19 People who habitually smoked cigarettes showed a higher prevalence of HCV infection than those who did not, and multivariate logistic regression showed smoking to be a significant risk factor for acquiring HCV infection.10 Cigarette smoking is also highly associated with the development of hepatocellular carcinoma.15,20 Nevertheless, the effect of smoking on the necroinflammatory activity of anti-HCV–seropositive patients is not fully understood. Smoking has been shown to influence all aspects of the immune systems, including alterations of humoral and cellular immunity.21 Further study is needed to determine whether cigarette smoking has effects similar to those of alcohol consumption on the increase of viral replication, the worsening of histological progression, and the immunosuppression within anti-HCV–seropositive individuals.

    In this study, the prevalence of elevated ALT levels was about 3 times higher for those who habitually smoked 1 PPD or more and frequently drank alcohol than for those who did neither. In addition, 75.2% of those anti-HCV–seropositive subjects who did not smoke cigarettes or drink alcohol had ALT levels within the normal range. The reason for a greater prevalence of normal ALT levels among these anti-HCV–seropositive individuals could be that more of them were seronegative for HCV RNA and they had less change in histological findings in the liver. As a result, they might be less liable to development of chronic disease than those who do consume cigarettes or alcohol.1,17,22 In addition, they might be more likely to recover from an acute HCV infection and become seronegative for HCV RNA because of better host immunity. A clear correlation exists between alcohol consumption and liver HCV RNA levels.9 Whether a correlation also exists between smoking levels and liver HCV RNA levels requires further study. The prevalence of cigarette smoking is much higher than that of alcohol consumption (27.2% vs 5.5%) in this study, but the effect of smoking on anti-HCV–seropositive people is almost overlooked in practice. It will be helpful for secondary prevention to suggest that anti-HCV–seropositive patients abstain from cigarette smoking as well as alcohol consumption.

    Confounding factors might exist in this study. First, because smokers might use health care services more often than nonsmokers,23 they might be given more medications or medical injections that could result in different genotypes of HCV infections or that could produce hepatic necroinflammation and thereby cause more elevated ALT levels.2 Second, smokers were more likely to have a lower socioeconomic status than nonsmokers and therefore were more likely to work in more hazardous environments that cause more elevated ALT levels.2

    Some limitations exist in this community-wide population study. First, because the amounts of cigarette and alcohol consumption were self-reported, a bias toward underestimation might exist due to social stigmata associated with the reporting of these adverse lifestyle practices. Misclassification of alcohol consumption might have occurred, because information about the amount of alcohol consumed was not obtained. Second, the duration of cigarette and alcohol consumption was not recorded, but duration is associated with liver damage that can cause elevated ALT levels. Third, polymerase chain reaction analysis for HCV RNA levels was not performed to elucidate the relationship between the actual viral status or viral titers and past infections. Finally, this cross-sectional study may blur etiologic associations; hence, a long-term prospective study is needed to see the effects of cigarette smoking, the combined effects of smoking and alcohol consumption, and the effects of abstinence on HCV infection.

    Alcohol and cigarette consumption are independently associated with elevated ALT levels among anti-HCV–seropositive individuals but not among HBsAg-seropositive individuals. This finding will be useful for secondary prevention among anti-HCV–seropositive patients to slow further progression into advanced liver diseases and to decrease excessive use of health care services. Abstention from cigarettes and alcohol by anti-HCV–seropositive patients might be a cost-effective measure before initiation of treatment for anti-HCV seropositivity. The detailed biological effect of smoking on the necroinflammation, viral loads, histological progression, and hepatocarcinogenesis among anti-HCV–seropositive patients needs further evaluation.

    Accepted for publication July 31, 2001.

    This study was supported by the C. T. Hsu Cancer Research Foundation, Taipei City, Taiwan.

    We thank the A-Lein Community Health Promotion Committee, Kaohsiung County, Taiwan; the staff and volunteers of the A-Lein Community Health Center, Kaohsiung County, for their assistance in data collection; and the Tainan Blood Center of the Chinese Blood Service Foundation, Tainan City, Taiwan, for assistance with laboratory analysis.

    Corresponding author and reprints: Pesus Chou, DrPH, National Yang-Ming University, Institute of Public Health, Shih-Pai, Taipei 112, Taiwan, Republic of China (e-mail: [email protected] or [email protected]mail.ncku.edu.tw).

    1.Hoofnagle
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     et al. for the MULTIVIRC Group, Factors associated with serum alanine transaminase activity in healthy subjects: consequences for the definition of normal values, for selection of blood donors, and for patients with chronic hepatitis C.  Hepatology. 1998;271213- 1219Google ScholarCrossref 6.Chien
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     P Comparison of HBV and HCV prevalence and risk factors in a community-based study.  Am J Trop Med Hyg. In press.Google Scholar11.Wang
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     P Using the prevalence of an elevated serum alanine aminotransferase level for identifying communities with a high prevalence of hepatitis C virus infection.  Arch Intern Med. 2001;161392- 394Google ScholarCrossref 14.Not Available, Stata Reference Manual.  Release 3. 5th ed. Santa Monica, Calif Computing Resource Center1992;Google Scholar15.Mukaiya
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     et al.  Association between high serum alanine aminotransferase levels and more rapid development and higher rate of incidence of hepatocellular carcinoma in patients with hepatitis C virus–associated cirrhosis.  Cancer. 1999;86589- 595Google ScholarCrossref 17.National Institutes of Health Consensus Development Program, National Institutes of Health Consensus Development Conference Panel statement: management of hepatitis C.  Hepatology. 1997;26
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    90,000 “Why are ALT and AST elevated in the blood, what does this mean?” – Yandex.Qu

    The abbreviation ALAT stands for an indicator of the blood enzymes alanine aminotransferase, AST – asparaginine aminotransferase. AST and ALT indicators are included in the biochemical blood test.

    They were discovered in medicine relatively recently. A blood test for AST and ALT is carried out jointly and, accordingly, their rate should be the same, and fully depend on each other.

    Such an indicator of analyzes as an increase in ALT and AST in the blood by 2 or more times should make one think about the occurrence of certain diseases.First you need to understand what ALT and AST are. What is the rate of these compounds in the blood and what should be done if at least one indicator is increased?

    What does an increase in ALT and AST above normal indicate?

    In adults, the content of ALT and AST in different organs is not the same, therefore, an increase in one of these enzymes may indicate a disease of a particular organ.

    • ALT (ALaT, alanine aminotransferase) – an enzyme that is found mainly in the cells of the liver, kidneys, muscles, heart (myocardium – heart muscle) and pancreas.When they are damaged, a large amount of ALT is released from the destroyed cells, which leads to an increase in its level in the blood.
    • AST (ASaT, aspartate aminotransferase) is an enzyme that is also found in the cells of the heart (in the myocardium), liver, muscles, nerve tissues, and to a lesser extent in the lungs, kidneys, and pancreas. Damage to the above organs leads to an increase in the level of AST in the blood.

    Basically, the rate of ALT and AST in the blood depends entirely on the work of the most important parenchymal organ – the liver, which performs functions such as:

    1. Protein synthesis.
    2. Production of biochemical substances necessary for the body.
    3. Detoxification – removal of toxic substances and poisons from the body.
    4. Storage of glycogen – a polysaccharide, which is necessary for the full functioning of the body.
    5. Regulation of biochemical reactions of synthesis and disintegration of most microparticles.

    Normal blood levels of ALT and AST depend on gender. In an adult woman, the level of ALT and AST does not exceed 31 U / L.In men, normal ALT does not exceed 45 U / L, and AST 47 U / L. Depending on the age of the child, the level of ALT and AST changes, while the ALT content should not be higher than 50 U / L, AST – 140 U / L (from birth to 5 days) and not more than 55 U / L for children under 9 years old.

    Depending on the equipment used for the study, it is possible to vary the norms and reference values ​​of the enzyme level. An increase in the rate of renewal of enzymes, cell damage lead to an increase in the level of transaminases in the blood.

    The reasons for the increase in ALT and AST

    Why are ALT and AST elevated in adults, what does this mean? The most likely reason for an increase in liver enzymes in the blood are:

    1. Hepatitis and other liver diseases (

      cirrhosis of the liver

      , fatty hepatosis – replacement of liver cells with fat cells, liver cancer, etc.).

    2. Increase in ALT and AST as a result of diseases of other organs (autoimmune thyroiditis, mononucleosis).
    3. Myocardial infarction

      – This is a necrosis (death) of a portion of the heart muscle, as a result of which ALT and AST are released into the blood.

    4. Diffuse liver damage that can be caused by alcohol, drugs and / or the action of a virus.
    5. Major injuries with muscle damage, as well as burns, cause an increase in ALT in the blood.
    6. Acute and chronic pancreatitis.
    7. Metastases or neoplasms in the liver.
    8. Drug reaction.
    9. Taking anabolic steroids.

    AST and ALT are important indicators of the state of various organs. An increase in these enzymes indicates damage to organs such as the liver, heart, muscles, pancreas, etc. Thus, a decrease in their level in the blood occurs on its own when the underlying disease is eliminated.

    Prophylaxis

    In order to ensure that the rate of indicators does not exceed the permissible limits, it is recommended to avoid long-term administration of drugs.

    If this is not possible due to a chronic disease, then it is better to regularly take an AST test so that it is not increased or a serious increase can be prevented in time. Periodically, you need to visit a gastroenterologist and hepatologist, who can identify a possible disease and prescribe treatment.

    What to do if ALT and AST are elevated

    In order to quickly and objectively understand the true reason for the increase in the levels of activity of the enzymes ALT and AST, it is necessary to additionally pass biochemical tests.

    First of all, it is advisable to determine

    total bilirubin levels

    , alkaline phosphatase and GGTP (gamma-glutamyltransferase) and assess the degree of safety of the main functions of the liver. To exclude the viral nature of liver damage (acute viral hepatitis), which is also accompanied by an increase in ALT and AST in the blood, you will need to donate blood for specific antigens of viral hepatitis and specific antibodies to these antigens.

    In some cases, it is shown that blood serum is tested by PCR for the presence of HBV DNA and HCV RNA.

    Material provided

    simptomy-lechenie.net

    increased asthma and altitude during pregnancy – 25 recommendations on Babyblog.ru

    This is my summary of the literature on this topic: how to detect, prevent preeclampsia …

    DIAGNOSTICS OF PREGESTOSIS: when there is no gestosis yet, it is necessary to identify a tendency to it:

    1. Risk group for the development of preeclampsia: careful dispensary observation than for women without somatic pathology.
    2. Revealing:
    • pathological weight gain after 20 weeks of gestation in the absence of visible edema.
    • An increase in diastolic pressure of more than 90 mm Hg
    • a decrease in pulse pressure to 30 or less.
    • Asymmetry of blood pressure in two arms (it is always necessary to measure it on two arms). Asymmetry more than 10 mm Hg.
    • functional tests for measuring blood pressure: a test with a turn – turn the woman to the left side, to the right, and if after that the change in blood pressure is more than 20 mm Hg, then this woman will be included in the risk group.
    • Decrease in daily urine output to 900 ml / day or less. In this case, a decrease in the specific gravity of urine is determined.
    • Mild proteinuria.
    • Higher average BP figures. The average blood pressure rate is 90-100 mm Hg, if more than 105 then this is a pathology.
    • Laboratory values ​​(hemoglobin, hematocrit, etc. see below).

    Various reasons that can affect the occurrence of gestosis (risk group):

    – diseases of internal organs;

    – overweight

    – lack of protein in the body;

    – edema during pregnancy;

    – early toxicosis;

    – weak nervous system;

    – pressure surges;

    – the emotional state of a pregnant woman.

    – problems with blood clotting, hereditary-acquired thrombophilia

    WHEN GESOSIS IS SUSPECTED (PREECLAMPSIA): if it seems to you that what is wrong with you is gestosis, you need to do the following checks

    Analyzes. To exclude preeclampsia, it is advisable to conduct a comprehensive examination – complete blood count, homocysteine ​​level, biochemical blood test (detailed), hemostasiogram, general urine analysis, in case of proteinuria – daily urine for protein, fetal ultrasound, dopplerometry, CTG.Also, before receiving an obstetrician-gynecologist, it is advisable to start daily weight control in the morning after using the toilet, control blood pressure 2 times a day, control the daily volume of consumed and released fluids.

    A decrease in the volume of circulating plasma was found already in the second half of pregnancy. An increase in blood pressure precedes an increase in hematocrit. Thrombocytopenia as a symptom of very severe preeclampsia appears before the symptoms of ARF. Doppler ultrasonography can reveal a violation of blood flow in the uteroplacental circle of blood circulation.Violation of the rheological properties of blood (increased viscosity) can be detected from 20 weeks, and the clinic may appear after 32-36 weeks. The use of dopplerometry can reveal impaired blood circulation from the 16th week of pregnancy: fetal growth retardation syndrome as a symptom of ORN – gestosis. Hypotension can be predicted in 64%.
    A decrease in prostacyclin synthesis is observed from the 20th week of pregnancy in women who develop preeclampsia.

    PREVENTION OF gestosis 90 100

    Before pregnancy:

    Reduce weight

    – find out the cause of gestosis if it was before:

    1.General blood test
    2. General urine test
    3. Biochemical blood test (Potassium, sodium, ALT, AST, kidney and liver markers)
    4. Blood test for infections (all the same as during pregnancy)
    5. Research blood test for hormones (thyroid, testosterone, etc.)
    6. Blood test for hemostasis, homocysteine ​​and mutations)
    7. Consultation with a hemostasiologist
    8. Ultrasound of the abdominal organs (especially the kidneys and adrenal glands)
    9. Ultrasound of the thyroid gland
    10.Endocrinologist’s consultation
    11. Brain vessels duplex
    12. Neurologist’s consultation
    13. ECG
    14. Cardiologist’s consultation

    – Examine internal organs (liver, kidneys, heart, pelvic organs)

    – Know the norms of pressure, urine, blood

    During pregnancy:

    – completely exclude table salt, replace it with sea salt.

    – protein food link (chicken or turkey)

    – nerves: valerian or other sedative

    – weight control for weeks on an empty stomach, after using the toilet (in order to identify weight gains)

    – pressure control 3 times a day (at the same time, an hour after eating, after sitting for 10 minutes at rest and in the same position, it is better to measure 3 times at a time on different hands): Women with a threat of developing toxicosis have higher average pressure.Average blood pressure is equal to syst. BP + 2distol. BP / 3

    – urine control (strip test)

    – blood control (signs of blood – low protein in the blood, increased hemoglobin (HGB) above 120 g / l, hematocrit (Ht)) normal total serum protein: 65-85 g / l, reducing it to 60 g / l already indicates severe gestosis; serum albumin is normally 35-55 g / l, with a decrease to 30 g / l edema develops; normal hematocrit 0.36 – 0.42 l / l

    – water 2.5 liters per day.

    – Folic acid, aspirin.

    link

    AFS ref.

    Vitamin e is useful for signs of preeclampsia

    From a practical point of view, it is not the severity of arterial hypertension that is dangerous, but complications associated with sharp fluctuations in blood pressure, which are the cause of fetal death, delay in development, hypoxia, premature birth, premature detachment of the normally located placenta. Therefore, if persistent hypertension of pregnant women is detected, they are hospitalized and the following treatment is prescribed:
    – bed rest in the lateral position in order to avoid aortocaval hypotension and provocation of renal ischemia;
    – sedatives that have a calming effect, suppress feelings of anxiety, internal tension, reduce anxiety;
    – antihypertensive drugs used in combination with drugs that improve intraplacental perfusion.

    When part of the placenta is preserved, gestosis is preserved.

    Girls who survived this horror, please answer the survey http://www.babyblog.ru/community/post/poteri/1692609

    90,000 What is the SGOT test?

    When the liver becomes damaged, enzymes known as aminotransferases are released more freely into the bloodstream. One type of these enzymes is called aspartate aminotransferase (AST), also called serum glutamic oxaloacetic transaminase (SGOT).Before prescribing certain medications or if liver disease is suspected, your doctor may order a routine blood test, called an SGOT test, to make sure the enzyme is not overly concentrated in the blood – a clear signal of deeper medical problems.

    Children or adults suspected of having liver disease or even hepatitis share a common set of symptoms. These include jaundiced or yellowed skin, dark yellow or even orange urine, frequent nausea and vomiting, and even a swollen stomach area.These symptoms can also be caused by certain types of medications that doctors need to be aware of before prescribing other medications. These medications can be antibiotics, pain relievers as common as aspirin and ibuprofen, or multiple medications prescribed to lower cholesterol, seizures, depression, and cardiovascular stress.

    The SGOT test will be ordered to determine if an excess amount of this enzyme is released into the blood, indicating that further testing is needed.SGOT or AST is present in several organs such as the heart, liver, kidneys, muscles, and even the brain. If a high level is found during the test, it could be due to damage to one or more of these organs.

    In contrast, another common liver enzyme called alanine aminotransferase (ALT) is found primarily in the liver. Also called serum glutamic pyruvic transaminase (SGPT), an ALT / SGPT blood test can help doctors determine if the liver or other organ has been damaged.Often the SGOT test includes an SGPT test.

    High ALT or AST levels found on an SGPT or SGOT test do not necessarily indicate liver damage. Certain types of muscle damage or tension can create higher levels of aminotransferases. Strains of viral hepatitis also cause these levels to rise, as do more rare disorders such as hemachromatosis, Wilson’s disease, celiac disease, and alcerative colitis. To get closer to a specific disorder, a red flag spotted during an SGPT or SGOT test often prompts doctors to order other tests.These are called the coagulation panel, albumin levels, platelet counts, and bilirubin tests, which more closely analyze the causes of liver damage.

    OTHER LANGUAGES

    ALCOHOLISM TEST – RUSSIAN DOCTOR IN THE TROPICS – LJ

    “Alcoholism” is a rather psychiatric concept and therefore not very practical.

    It would seem, what is easier? – if there is a mental and / or physical dependence on ethyl alcohol (that is, alcohol), then alcoholism is on your face! In practice, everything is more complicated.Alcoholics, like all people with addictions, are very rarely aware of their problem and do not want to go to surrender to narcologists. But even the narcologists themselves are in no hurry to establish a stigmatizing diagnosis until they are completely pinned down, and the patient is not hospitalized with delirium tremens.

    As a result, alcoholism in Russia, and in other countries, is diagnosed much less often during life than on the table of a pathologist who, with routine sadness, shreds the cirrhotic liver and describes other organ changes characteristic of long-term drunkenness.

    If we compare serious statistical data, it turns out that in Russia at least 15% of men die by alcoholics, including for reasons directly related to alcohol dependence (cirrhosis of the liver, suicide in a state of delirium = fever, drunken injuries) … For a number of regions, this figure reaches 20%, i.e. every 5th man there is a real alcoholic! France and Germany are not inferior to us in statistics.

    So how do you know if you or your loved one is in danger?

    fakeFCKRemove

    So, let’s leave the diagnosis “alcoholism” to the narcologists, let them tinker with it. It is much more important for us to exclude the other – alcohol abuse!

    By alcohol abuse I mean the use of such doses of ethanol that lead to liver necrosis . Regular such necrosis trigger the entire cascade of changes leading to cirrhotic degeneration of the organ (ie, when the liver tissue is replaced by fibrous “scars” that overgrow the areas of necrosis, as a result of which there are so few liver cells that a person literally remains without a liver).

    So by necrosis of these alcohol abuse is very easy to diagnose !

    We go to the laboratory and ask to do a biochemical test for the hepatic enzyme GGT (gamma-glutamyl transpeptidase). This test is extremely sensitive to ethanol liver damage!

    So:

    • If you get a normal value (up to 40 U / l), you don’t need to steam – you don’t abuse alcohol :).
    • If the value is high, ALT (alanine aminotransferase = transpeptidase) should be checked.If ALT is also increased, we look at exactly how it is increased:
      – if it does not exceed the values ​​of GGT, then we tend to think about alcohol;
      – if it significantly overlaps the GGT figures, then we think more about viral liver damage and run to do a test for markers to hepatitis B and C.
      – if all liver enzymes are slightly increased somewhere in the same degree, we also think about other rare liver lesions ( parasites, rare genetic diseases, mysterious TTV virus, hepatotoxic drugs, etc.).

      I must say right away that if markers for hepatitis viruses turn out to be negative, your GGT is increased due to alcohol with a probability of 95%, and you need to quit, and not run to doctors looking for a mythical disease.

      Since the GGT test is very sensitive, it can jump even from a single binge (at a wedding, funeral, about the birth of a nephew, dismissal, promotion, Bilan’s victory at Eurovision, etc.), when the liver receives a completely unexpected blow.Then we can only talk about episodic alcohol abuse without the formation of more dependence. How to confirm this?

      Easier than a steamed turnip! We wait a month, completely abstain from alcohol, and again donate blood for GGT:

    • If the test is increased, despite the fact that you did not drink a drop, we carry out differential diagnostics (since the test is not strictly specific for alcohol cases) : We go to a gastroenterologist (better to a hepatologist) to do an ultrasound of the liver or other tests, suddenly they find some kind of echinococcus.
    • If GGT has returned to normal, then it was just an episode.
    • If you fell, but still far from the ideal value, then these occasional drinking bouts were not so rare, and you are one step away from the formation of alcohol addiction!
    • If you were unable to abstain from alcohol for a whole month (no matter for what reason), and therefore the test remained at the same high level, then you are addicted to alcohol (that is, already an alcoholic), and your train left …

      Now for some theory.
      Such alcoholic liver disease, when cirrhosis has not yet formed, but the enzymes are already high, is called alcoholic steatohepatitis , i.e. inflammation of the liver with its simultaneous fatty transformation, caused by toxic metabolites of alcohol.

      In alcoholic steatohepatitis, hepatic cells of hepatocytes die with the formation of areas of necrosis. During their death, the enzymes GGT, ALT and AST contained in them are released into the blood. It was then that the laboratory detects them.

      This disease is not uncommon, as you already understood, but for some reason in Russia it is practically not diagnosed, for fear of offending a person with a diagnosis of “alcoholic”.According to the soviet tradition, the use of the word “alcoholic” remains with us the prerogative of narcologists, although it is a no brainer that the narcologist knows little about hepatitis and cirrhosis. At the same time, it is liver damage in alcohol abuse and alcoholism that is the leading and ultimately defining symptom! Our therapists, looking at the overwhelming enzymes, simply shrug their shoulders and carry any blizzard about the wrong diet and the need to drip Essentiale, beloved by the people, etc. etc.

      In advanced alcoholics who have reached the 2nd stage, when physical dependence with its withdrawal hangover syndrome is already forming, the following picture appears in biochemical analyzes:
      – GGT is greatly increased (more than 150-200 U / l)
      – ALT is slightly increased (2-3 times from the norm)
      – blood triglycerides (fats) are increased, i.e.because alcohol at this stage already disrupts the metabolism of fatty acids in the liver, and it begins to grow fat (fatty degeneration in alcoholics goes along with necrotic fibrosis)
      – increased blood uric acid, because alcohol greatly disrupts the exchange of purine bases, which by the 3rd stage will lead to gout.

      I see the above picture quite often when I solve expert questions on the professional suitability of Russian workers. Now more and more serious companies are introducing the GGT test as a mandatory component of medical examinations.And in such companies, it is alcohol abuse that becomes the most common medical reason for rejecting a candidate for employment.

      P.S .: No, , even the most terrible diet, does not affect the performance of liver enzymes . Blood for these indicators can be donated and not on an empty stomach.
      P.P.S .: All liver enzymes can increase, along with blood sugar, and other indicators in severe obesity, when already about overeating and the liver becomes obese, and diabetes mellitus develops and blood pressure rises, etc.

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