Normal enzyme count in liver: High, Low & Normal Results, Symptoms & Causes
Liver Enzyme – an overview
Liver enzymes, such as aspartate aminotransferase (AST) and alanine aminotransferase (ALT), are the most sensitive indicators of hepatocyte injury. Both AST and ALT are normally present in low concentrations. However, with cellular injury or changes in cell membrane permeability, these enzymes leak into circulation. Of the two, the ALT is the more sensitive and specific test for hepatocyte injury as AST can be also elevated in the state of cardiac arrest or muscle injury. Serum glutamate dehydrogenase (GLDH) is also a marker and is elevated in the state of severe hepatic damage. Serum alkaline phosphatase (ALKP) provides an elevation of the patency of the bile channels at all levels, intrahepatic and extrahepatic. Elevation is demonstrated in patients with obstruction of the extrahepatic biliary tract or caliculi. In general, serum levels are elevated in hepatobiliary disease.106
As mentioned earlier liver damage occurs after a thermal injury. The elevation of hepatic enzymes correlates with the severity and extend of the hepatic injury. Small hepatic injury leads to a predominantly elevation of the cytoplasmatic enzymes ALT and only little elevation of AST. The so-called de Ritis ratio GOT/GPT <1. In a state of severe hepatic damage, mitochondrial bound enzymes are strongly elevated and the de Ritis ratio GOT/GPT >1 (Table 26.3).106
Thermal injury causes liver damage by edema formation, hypoperfusion, pro-inflammatory cytokines or other cell death signals with the release of the hepatic enzymes. Others and we have shown that serum AST, ALT and ALKP are elevated between 50 to 200% when compared with normal levels (Figure 26.9). We observed that serum AST and ALT peaked during the first day postburn and ALKP during the second day postburn. During hepatic regeneration all enzymes returned to baseline between 10–14 days postburn. If liver damage persists, enzymes stay elevated. There is no need for therapeutic intervention to decrease elevated enzymes. Enzymes can only be used as markers and the effect of therapeutics can be studied.
The association of higher levels of within-normal-limits liver enzymes and the prevalence of the metabolic syndrome | Cardiovascular Diabetology
Dekker JM, Girman C, Rhodes T, Nijpels G, Stehouwer CD, Bouter LM, Heine RJ: Metabolic syndrome and 10-year cardiovascular disease risk in the Hoorn Study. Circulation. 2005, 112: 666-673. 10.1161/CIRCULATIONAHA.104.516948.
Jeppesen J, Hansen TW, Rasmussen S, Ibsen H, Torp-Pedersen C, Madsbad S: Insulin resistance, the metabolic syndrome, and risk of incident cardiovascular disease: a population-based study. J Am Coll Cardiol. 2007, 49: 2112-2119. 10.1016/j.jacc.2007.01.088.
Lakka HM, Laaksonen DE, Lakka TA, Niskanen LK, Kumpusalo E, Tuomilehto J, Salonen JT: The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. Jama. 2002, 288: 2709-2716. 10.1001/jama.288.21.2709.
Malik S, Wong ND, Franklin SS, Kamath TV, L’Italien GJ, Pio JR, Williams GR: Impact of the metabolic syndrome on mortality from coronary heart disease, cardiovascular disease, and all causes in United States adults. Circulation. 2004, 110: 1245-1250. 10.1161/01.CIR.0000140677.20606.0E.
Devers MC, Campbell S, Shaw J, Zimmet P, Simmons D: Should liver function tests be included in definitions of metabolic syndrome? Evidence from the association between liver function tests, components of metabolic syndrome and prevalent cardiovascular disease. Diabet Med. 2008, 25: 523-529. 10.1111/j.1464-5491.2008.02408.x.
Andre P, Balkau B, Vol S, Charles MA, Eschwege E: Gamma-glutamyltransferase activity and development of the metabolic syndrome (International Diabetes Federation Definition) in middle-aged men and women: Data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR) cohort. Diabetes Care. 2007, 30: 2355-2361. 10.2337/dc07-0440.
Nannipieri M, Gonzales C, Baldi S, Posadas R, Williams K, Haffner SM, Stern MP, Ferrannini E: Liver enzymes, the metabolic syndrome, and incident diabetes: the Mexico City diabetes study. Diabetes Care. 2005, 28: 1757-1762. 10.2337/diacare.28.7.1757.
Hanley AJ, Williams K, Festa A, Wagenknecht LE, D’Agostino RB, Haffner SM: Liver markers and development of the metabolic syndrome: the insulin resistance atherosclerosis study. Diabetes. 2005, 54: 3140-3147. 10.2337/diabetes.54.11.3140.
Liangpunsakul S, Chalasani N: Unexplained elevations in alanine aminotransferase in individuals with the metabolic syndrome: results from the third National Health and Nutrition Survey (NHANES III). Am J Med Sci. 2005, 329: 111-116. 10.1097/00000441-200503000-00001.
Goessling W, Massaro JM, Vasan RS, D’Agostino RB, Ellison RC, Fox CS: Aminotransferase Levels and 20-Year Risk of Metabolic Syndrome, Diabetes, and Cardiovascular Disease. Gastroenterology. 2008, 135 (6): 1935-44. 10.1053/j.gastro.2008.09.018. 1944.e
Emdin M, Passino C, Michelassi C, Titta F, L’Abbate A, Donato L, Pompella A, Paolicchi A: Prognostic value of serum gamma-glutamyl transferase activity after myocardial infarction. Eur Heart J. 2001, 22: 1802-1807. 10.1053/euhj.2001.2807.
Jousilahti P, Rastenyte D, Tuomilehto J: Serum gamma-glutamyl transferase, self-reported alcohol drinking, and the risk of stroke. Stroke. 2000, 31: 1851-1855.
Lee DH, Silventoinen K, Hu G, Jacobs DR, Jousilahti P, Sundvall J, Tuomilehto J: Serum gamma-glutamyltransferase predicts non-fatal myocardial infarction and fatal coronary heart disease among 28,838 middle-aged men and women. Eur Heart J. 2006, 27: 2170-2176. 10.1093/eurheartj/ehl086.
Lee DS, Evans JC, Robins SJ, Wilson PW, Albano I, Fox CS, Wang TJ, Benjamin EJ, D’Agostino RB, Vasan RS: Gamma glutamyl transferase and metabolic syndrome, cardiovascular disease, and mortality risk: the Framingham Heart Study. Arterioscler Thromb Vasc Biol. 2007, 27: 127-133. 10.1161/01.ATV.0000251993.20372.40.
Meisinger C, Doring A, Schneider A, Lowel H: Serum gamma-glutamyltransferase is a predictor of incident coronary events in apparently healthy men from the general population. Atherosclerosis. 2006, 189: 297-302. 10.1016/j.atherosclerosis.2006.01.010.
Ruttmann E, Brant LJ, Concin H, Diem G, Rapp K, Ulmer H: Gamma-glutamyltransferase as a risk factor for cardiovascular disease mortality: an epidemiological investigation in a cohort of 163,944 Austrian adults. Circulation. 2005, 112: 2130-2137. 10.1161/CIRCULATIONAHA.105.552547.
Wannamethee G, Ebrahim S, Shaper AG: Gamma-glutamyltransferase: determinants and association with mortality from ischemic heart disease and all causes. Am J Epidemiol. 1995, 142: 699-708.
Turgut O, Yilmaz A, Yalta K, Karadas F, Birhan Yilmaz M: gamma-Glutamyltransferase is a promising biomarker for cardiovascular risk. Medical hypotheses. 2006, 67: 1060-1064. 10.1016/j.mehy.2006.04.010.
Fraser A, Harris R, Sattar N, Ebrahim S, Davey Smith G, Lawlor DA: Alanine aminotransferase, gamma-glutamyltransferase, and incident diabetes: the British Women’s Heart and Health Study and meta-analysis. Diabetes Care. 2009, 32: 741-750. 10.2337/dc08-1870.
Ekstedt M, Franzen LE, Mathiesen UL, Thorelius L, Holmqvist M, Bodemar G, Kechagias S: Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology. 2006, 44: 865-873. 10.1002/hep.21327.
Kain K, Carter AM, Grant PJ, Scott EM: Alanine aminotransferase is associated with atherothrombotic risk factors in a British South Asian population. J Thromb Haemost. 2008, 6: 737-741. 10.1111/j.1538-7836.2008.02935.x.
Sattar N, Scherbakova O, Ford I, O’Reilly DS, Stanley A, Forrest E, Macfarlane PW, Packard CJ, Cobbe SM, Shepherd J: Elevated alanine aminotransferase predicts new-onset type 2 diabetes independently of classical risk factors, metabolic syndrome, and C-reactive protein in the west of Scotland coronary prevention study. Diabetes. 2004, 53: 2855-2860. 10.2337/diabetes.53.11.2855.
Steinvil A, Berliner S, Bromberg M, Cohen M, Shalev V, Shapira I, Rogowski O: Micro-inflammatory changes in asymptomatic healthy adults during bouts of respiratory tract infections in the community: potential triggers for atherothrombotic events. Atherosclerosis. 2009, 206: 270-275. 10.1016/j.atherosclerosis.2009.01.045.
Rogowski O, Steinvil A, Berliner S, Cohen M, Saar N, Ben-Bassat OK, Shapira I: Elevated resting heart rate is associated with the metabolic syndrome. Cardiovasc Diabetol. 2009, 8: 55-10.1186/1475-2840-8-55.
Rogowski O, Shapira I, Steinvil A, Berliner S: Low-grade inflammation in individuals with the hypertriglyceridemic waist phenotype: another feature of the atherogenic dysmetabolism. Metabolism. 2009, 58: 661-667. 10.1016/j.metabol.2009.01.005.
Rogowski O, Shapira I, Peretz H, Berliner S: Glycohaemoglobin as a determinant of increased fibrinogen concentrations and low-grade inflammation in apparently healthy nondiabetic individuals. Clin Endocrinol (Oxf). 2008, 68: 182-189.
Rogowski O, Shapira I, Shirom A, Melamed S, Toker S, Berliner S: Heart rate and microinflammation in men: a relevant atherothrombotic link. Heart. 2007, 93: 940-944. 10.1136/hrt.2006.101949.
Rogowski O, Toker S, Shapira I, Melamed S, Shirom A, Zeltser D, Berliner S: Values of high-sensitivity C-reactive protein in each month of the year in apparently healthy individuals. Am J Cardiol. 2005, 95: 152-155. 10.1016/j.amjcard.2004.08.086.
Steinvil A, Shirom A, Melamed S, Toker S, Justo D, Saar N, Shapira I, Berliner S, Rogowski O: Relation of educational level to inflammation-sensitive biomarker level. Am J Cardiol. 2008, 102: 1034-1039. 10.1016/j.amjcard.2008.05.055.
Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). Jama. 2001, 285: 2486-2497. 10.1001/jama.285.19.2486.
Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC: Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009, 120: 1640-1645. 10.1161/CIRCULATIONAHA.109.192644.
Barham D, Trinder P: An improved colour reagent for the determination of blood glucose by the oxidase system. Analyst. 1972, 97: 142-145. 10.1039/an9729700142.
Fossati P, Prencipe L: Serum triglycerides determined colorimetrically with an enzyme that produces hydrogen peroxide. Clin Chem. 1982, 28: 2077-2080.
Izawa S, Okada M, Matsui H, Hotta Y, Hama H: A new direct method for measuring HDL-cholesterol which does not produce any biased values. Jpn J Med Pharm Sci. 1997, 37: 1385-1388.
Szasz G: Reaction-rate method for gamma-glutamyltransferase activity in serum. Clin Chem. 1976, 22: 2051-2055.
Bergmeyer HU, Horder M: International federation of clinical chemistry. Scientific committee. Expert panel on enzymes. IFCC document stage 2, draft 1; 1979-11-19 with a view to an IFCC recommendation. IFCC methods for the measurement of catalytic concentration of enzymes. Part 3. IFCC method for alanine aminotransferase. J Clin Chem Clin Biochem. 1980, 18: 521-534.
Kotronen A, Westerbacka J, Bergholm R, Pietilainen KH, Yki-Jarvinen H: Liver fat in the metabolic syndrome. J Clin Endocrinol Metab. 2007, 92: 3490-3497. 10.1210/jc.2007-0482.
Paolicchi A, Emdin M, Passino C, Lorenzini E, Titta F, Marchi S, Malvaldi G, Pompella A: Beta-lipoprotein- and LDL-associated serum gamma-glutamyltransferase in patients with coronary atherosclerosis. Atherosclerosis. 2006, 186: 80-85. 10.1016/j.atherosclerosis.2005.07.012.
Anderson ME, Allison RD, Meister A: Interconversion of leukotrienes catalyzed by purified gamma-glutamyl transpeptidase: concomitant formation of leukotriene D4 and gamma-glutamyl amino acids. Proc Natl Acad Sci USA. 1982, 79: 1088-1091. 10.1073/pnas.79.4.1088.
Despres JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, Larose E, Rodes-Cabau J, Bertrand OF, Poirier P: Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk. Arterioscler Thromb Vasc Biol. 2008, 28: 1039-1049. 10.1161/ATVBAHA.107.159228.
Tenenbaum A, Fisman EZ, Motro M: Metabolic syndrome and type 2 diabetes mellitus: focus on peroxisome proliferator activated receptors (PPAR). Cardiovascular diabetology. 2003, 2: 4-10.1186/1475-2840-2-4.
Patel DA, Srinivasan SR, Xu JH, Chen W, Berenson GS: Persistent elevation of liver function enzymes within the reference range is associated with increased cardiovascular risk in young adults: the Bogalusa Heart Study. Metabolism. 2007, 56: 792-798. 10.1016/j.metabol.2007.01.010.
My dog has an elevated alkaline phosphatase. What does that mean? – Southwest Journal
There are several liver enzymes that veterinarians will check on a routine basis. The two most common liver enzymes checked are called ALT (alanine aminotransferase) and ALP (alkaline phosphatase). These enzymes come from different places in the liver, so the level of concern your veterinarian will have for your dog will vary depending on which enzyme is elevated and to what degree.
ALT should be tucked inside of the liver cell. When it comes out into the blood at higher than normal levels, this indicates that something is irritating the liver cell membrane, allowing the enzyme to leak out of the cell. Vets become concerned when this enzyme gets too high because it means that something is irritating or damaging the liver. There are a variety of reasons this enzyme can go up: infection, inflammation, toxin ingestion, a tumor and copper storage disease are all on veterinarians’ “rule-out” lists. (Copper storage disease is a condition in which the body traps copper in the liver). A normal range for this enzyme is around 18–120 U/L (normal ranges vary by lab) and mild elevation in this enzyme is not uncommon, especially in older animals. Every veterinarian has a different comfort level for when to worry about this enzyme. For me, I start to get more concerned when the reading goes above 200.
ALP comes from a totally different spot in the liver, and changes in this liver enzyme typically cause less concern for veterinarians. (ALP also comes from the bone, so this enzyme is not liver specific. For the scope of this article, however, we will discuss ALP made by the liver). This enzyme is made on the liver cell membrane, and there are a variety of factors that can stimulate the liver to make more of this enzyme. The normal range for this enzyme is 5–160 U/L. For me, I start to get more concerned when this enzyme goes above 500. It is common to see this enzyme become very elevated in dogs that are otherwise acting normally. I have some patients that have an ALP in the 1,000–2,000 range and clinically appear healthy.
There are a variety of reasons that the liver will make more ALP enzyme. One common reason is that the aging liver will sometimes develop benign areas of liver growth called nodular hyperplasia. (You have probably heard that your ears and nose keep growing as you get older – so too will your liver grow new cells over time.) If there are more liver cells to make more of this enzyme, then the ALP will increase.
Another common reason for an older animal to have an elevated ALP is if they have Cushing’s disease. Cushing’s disease (hyperadrenocorticism) is where the adrenal glands are producing more hormone then they should. These adrenal hormones influence the liver and turn on production of ALP.
Certain medications can also turn on production of ALP. One of the most notable medications that does this is a seizure medication called phenobarbital. Phenobarbital can benignly cause an elevated ALP, but this medication can also cause liver damage. Because of this, it is common for veterinarians to want to do more testing on the liver if a dog has an elevated ALP and is taking phenobarbital so she can differentiate between a benign and toxic liver change.
It is not always a benign reason that the ALP is up. For example, the ALP will also go up in dogs if there is a gallbladder or bile problem, or a tumor in the liver. Interpreting liver enzyme elevation is where the “Art of Medicine” comes in and the practitioner must take in the big picture of the pet and the desires of the client. If the pet is clinically normal, then monitoring may be recommended. If the pet is acting sick (drinking more, not eating, vomiting, panting or otherwise seeming unwell), or the client wants more information, then the practitioner may recommend further testing, like a liver ultrasound.
Clinical Approach to Elevated Liver Enzyme Activities
Internal Medicine Clinical Update:
Clinical Approach to Elevated Liver Enzymes
Michael Goldstein, DVM, Diplomate ACVIM
Central Toronto Veterinary Referral/Emergency Clinic
Elevated liver enzymes are a common finding noted in blood work performed on both healthy and ill dogs and cats. One study documented elevated alkaline phosphatase (ALP) concentrations in up to 40% of dogs with elevated liver enzymes. However, the finding of elevated liver enzymes does not always mean that there is significant primary liver disease. Therefore, as clinicians we must evaluate the history and undertake physical examination (PE) to determine the significance of the elevation in order to determine a diagnosis and create a treatment plan.
There are two major categories to classify liver enzymes: hepatocellular leakage (Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST)) and cholestatic/induction enzymes (ALP and Gamma-Glutamyltransferase (GGT)).
ALT is primarily located in the cytoplasm of the liver cells, whereas AST is found in abundance in a variety of tissues, most notably skeletal muscles. Both of these aminotransferases rapidly leak out of the hepatocyte when there is altered permeability from injury or metabolic disturbance. The magnitude of elevation correlates with the number of hepatocytes involved but does not reflect the overall functional capacity of the liver. This vital organ has an immense reserve capacity and as such animals with marked enzyme elevations may still have enough liver function to prevent clinical disease from becoming apparent.
ALP and GGT are membrane-bound enzymes and need to be cleaved from the membrane before becoming elevated in the blood. As such, there can be a delay between elevation in the aminotransferases and cholestatic/induction enzymes. There are multiple forms of ALP but the most clinically significant forms are bone (B-ALP), liver (L-ALP), and glucocorticoid (G-ALP). The G-ALP has little to no effect in cats but in conjunction with the L-ALP has been found to be associated with hepatobiliary disease, endocrine disorders, and pancreatitis in dogs. GGT is more sensitive but less specific than ALP in cats for hepatobiliary disease. I often use GGT when attempting to determine the cause of hepatic lipidosis in cats, since an elevated ALP and normal GGT concentration is consistent with primary hepatic lipidosis.
My general rules of interpretation of liver enzymes:
- 2-3 fold increases in ALT/AST concentration in healthy pets
- Revisit patient history, drugs, supplements, etc.
- Recheck in 2 to 3 weeks
- 3 fold increases in ALT/AST, history, and PE suggest a problem
- Liver function tests pre- and post-prandial bile acids
- If bile acids are abnormal then ultrasound and possible liver biopsy
- The degree of elevation in the ALP does not correspond to the degree of illness
- If a patient has no clinical signs and only an ALP elevation then it does not need to be evaluated for Cushing’s disease
If you have questions regarding liver disease or any Internal Medicine cases please do not hesitate to contact Dr. Michael Goldstein, Dr. Stephen Kruth or Dr. Kimberly Ho for a free, no obligation phone consultation at 416-784-4444 ext 1 and follow the prompts.
Thank you for being part of our circle of care.
Posted by: Michael Goldstein, DVM, Diplomate ACVIM
Categorised as: Clinical Updates
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Increased bilirubin in the blood: which means, the norm of indicators
Bilirubin in the blood: what does the increased indicators mean
Increased bilirubin in the blood: which means the norm of indicators
Bilirubin in the blood: which means increased levels
Bilirubin is a substance that is formed in the human liver as a result of the breakdown of proteins. About what the elevated bilirubin in the blood means, what are the reasons… RIA Novosti, 24.08.2021
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MOSCOW, Aug 20 – RIA Novosti. Bilirubin is a substance that is formed in the human liver as a result of the breakdown of proteins.About what the elevated bilirubin in the blood means, what are the reasons for this, the rate of indicators, what is the difference between total, direct and free bilirubin – in the material of RIA Novosti. What is bilirubin? Bilirubin is a pigment that is the main component of bile in the body. Its indicators reflect the work of enzymes in the liver. If its level is increased, then this can lead to a number of diseases and cause problems with the functioning of this organ. Formation of bilirubin Bilirubin appears in the body as a result of the breakdown of hemoglobin proteins, etc.As a result, it is excreted with the help of bile. Norms of indicators There are norms of indicators of bilirubin in the body, which vary depending on its type: Direct and indirect (free) bilirubin Direct bilirubin is a substance that passed through the liver, bound with glucuronic acid and lost its toxicity … It is excreted by the body through the intestines and kidneys. “Direct bilirubin is present in minimal concentrations in the body, because small quantities of red blood cells can be destroyed in the spleen, blood vessels, tissues, and not only in the liver,” the expert explained.- But if its level exceeds the norm, it means that the body did not bind it with glucuronic acid and turned it into indirect bilirubin. Free bilirubin is toxic to all organs, including the brain. It penetrates very well into cells, disrupting their vital functions, and into tissues, staining them. The jaundice color of the skin with hepatitis is precisely the result of the action of free bilirubin. If the substance gets into the brain, then this is the worst, because it cannot remove bilirubin, since it is not intended for this.Then there is the likelihood of developing a bilirubin coma. A person turns off, because there is such a high amount of substance in the body that he cannot do anything about it, and then he dies. Therefore, there should not be an excess of free bilirubin in the body, but only within the minimum concentration. “Total bilirubin. Total bilirubin consists of indirect and direct.” with a violation of bilirubin, – added a clinical pharmacologist.- It can be hepatitis (A, B, C, etc.), liver dysfunction associated with medications, drug hepatitis. In general, when there are liver diseases, bilirubin always manifests itself. ” and feces, – said Andrey Kondrakhin. – In the blood, total bilirubin is determined, in urine – urobilinogen (a colorless product of bilirubin reduction, formed under the action of intestinal bacteria – Approx.ed.). Increased indicators indicate that there are liver problems associated with the metabolism of bilirubin. At the same time, in 90% of cases, people are faced with liver diseases. ” the body, a tumor is formed in the liver, helminths start up in the body, an insufficient amount of enzymes is produced, etc.In addition, a high content of bile pigment can also be associated with infectious inflammation, intoxication, and hepatitis. According to Andrei Kondrakhin, the destruction of erythrocytes can affect the increased bilirubin. The new coronavirus infection also affects the liver, therefore, after the illness, you should undergo an examination, be tested for the level of bilirubin in the body. …This leads to organ dysfunction, patients develop jaundice, the pigment is able to penetrate into the brain tissue, cause damage to the nervous system (encephalopathy), which can manifest itself as impaired consciousness, hyperexcitability syndrome, convulsions, delayed psychomotor development. a symptom and, perhaps, leading, before the skin begins to turn yellow, is the appearance of dark urine, or, on the contrary, it becomes like water, – Andrey Kondrakhin commented.- It all depends on what kind of jaundice has arisen. If it is obstructive jaundice, then bilirubin does not enter the intestines, so the color of urine and feces is light. If it is hepatitis, then the excrement will be dark. “With a high content of bilirubin in the blood, the following manifestations are possible: Treatment To bring the level of bilirubin in the blood back to normal, it is necessary to eliminate the underlying disease. , medications, phototherapy by radiation, you should also change your diet.”There is gallstone disease, when a stone forms in the gallbladder,” the clinical pharmacologist added. If the patient is not operated on in time, then bilirubin will stagnate in the bile ducts, in the future it will lead to an enlargement of the liver, cirrhosis will occur – the destruction of its cells.After the procedure, bile is not absorbed anywhere and the body begins to function normally. If we talk about infectious diseases, they are treated by infectious disease specialists, for example, all hepatitis. Patients are prescribed various drugs, including those that improve liver function. “
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MOSCOW, 20 Aug – RIA Novosti. Bilirubin is a substance produced in the human liver as a result of the breakdown of proteins. About what the elevated bilirubin in the blood means, what are the reasons for this, the rate of indicators, how the total, direct and free bilirubin differ – in the material of RIA Novosti.
Bilirubin what is it?
Bilirubin is a pigment that is the main component of bile in the body. Its indicators reflect the work of enzymes in the liver. If its level is increased, then it can lead to a number of diseases and cause problems with the functioning of this organ.
Formation of bilirubin
Bilirubin appears in the body as a result of the breakdown of hemoglobin proteins, etc. As a result, it is excreted using bile.
“Bilirubin is formed in the liver when erythrocytes age and are destroyed,” Andrey Kondrakhin, PhD, clinical pharmacologist, told RIA Novosti. everything else in the form of bile pigment in the body begins to bind. As a result, bilirubin is utilized through feces and urine. Bilirubin is a toxic substance, therefore it is considered one of the main markers of liver health. “
Norms of indicators
There are norms of indicators of bilirubin in the body, which vary depending on its type:
direct bilirubin. Its normal level in the blood is from 0 to 5.1 μmol / L;
indirect (free) bilirubin. Its level in blood plasma should not be higher than 16.4 μmol / l;
total bilirubin. In a healthy person, its norm in the blood is from 0.5 to 20.5 μmol / l
Seven most dangerous products for the liver are named
Direct and indirect (free) bilirubin
Direct bilirubin is a substance that has passed through the liver , bound to glucuronic acid and lost toxicity.It is excreted by the body through the intestines and kidneys.
“Direct bilirubin in minimal concentrations is present in the body, because red blood cells in small quantities can be destroyed in the spleen, blood vessels, tissues, and not only in the liver,” the expert explained. “But if its level exceeds the norm, it means that the body did not bind it with glucuronic acid and turned it into indirect bilirubin.Free bilirubin is toxic to all organs, including the brain.It penetrates very well into cells, disrupting their vital functions, and into tissues, staining them. The jaundice color of the skin with hepatitis is precisely the result of the action of free bilirubin. If the substance gets into the brain, then this is the worst, because it cannot remove bilirubin, since it is not intended for this. Then there is the likelihood of developing a bilirubin coma. A person turns off, because there is such a high amount of substance in the body that he cannot do anything about it, and then he dies.Therefore, there should not be an excess of free bilirubin in the body, but only within the minimum concentration. “
Total bilirubin consists of indirect and direct. a person has any liver disease associated with a violation of bilirubin, added the clinical pharmacologist. – It can be hepatitis (A, B, C, etc.), liver dysfunction associated with medications, drug hepatitis.In general, when there is liver disease, bilirubin always manifests itself. ”
“There are three analyzes – blood, urine and feces,” said Andrey Kondrakhin. – In the blood, total bilirubin is determined, in urine – urobilinogen (a colorless product of bilirubin reduction, formed under the action of intestinal bacteria – Approx.ed.). Increased indicators indicate that there are liver problems associated with the metabolism of bilirubin. At the same time, in 90% of cases, people are faced with liver diseases. ” , primary biliary cirrhosis is formed, cholelithiasis develops or other pathologies arise that prevent the outflow of bile from the body, a tumor forms in the liver, helminths are produced in the body, an insufficient amount of enzymes is produced, etc.In addition, a high content of bile pigment can also be associated with infectious inflammation, intoxication, and hepatitis. According to Andrei Kondrakhin, the destruction of erythrocytes can affect the increased bilirubin.
“It can occur due to poisoning with mushrooms, surrogate drinks. There is such a disease as hemolytic disease of newborns, when the mother’s own antibodies fight with the baby’s erythrocytes, destroying them. Hemolysis can also occur due to poisoning with external poisons, for example, acetone. , paint, that is, if the concentration is exceeded, erythrocytes will begin to die.It can also be chemicals that are ingested, radiation damage, Rh-conflict between mother and child, congenital diseases, malaria, in which red blood cells also break down, “the specialist explained.
A new coronavirus infection also affects the liver, therefore after an illness, you should undergo an examination, be tested for the level of bilirubin in the body.
“Now, if a person is sick with a coronavirus infection, he takes many drugs, and the toxic effect of the virus leads to liver dysfunction,” added the clinical pharmacologist.- Because of this, some people may have an increase in bilirubin. In addition, in alcohol abusers, the liver is loaded, due to this, the organ becomes large and friable, and fatty hepatosis may occur. In this case, there is a violation of protein metabolism, so direct bilirubin ceases to bind to protein, because of this, a person may develop alcoholic hepatitis. “This leads to disruption of the functioning of organs, patients develop jaundice, the pigment is able to penetrate into the brain tissue, cause damage to the nervous system (encephalopathy), which can manifest itself as impaired consciousness, hyperexcitability syndrome, convulsions, delayed psychomotor development.
Symptoms of increased indices
“The very first symptom and, perhaps, the leading one, before the skin begins to turn yellow, is the appearance of dark urine, or, on the contrary, it becomes like water,” commented Andrey Kondrakhin.- It all depends on what kind of jaundice has arisen. If it is obstructive jaundice, then bilirubin does not enter the intestines, so the color of urine and feces is light. If it is hepatitis, then the excrement will be dark. “
With a high content of bilirubin in the blood, the following manifestations are possible:
an unnatural skin tone appears – from bright yellow to greenish;
skin itching occurs;
a bitter taste is felt in the mouth;
feces become white;
memory is impaired;
the liver increases in size, there is heaviness in the right side;
weakness is felt.
To normalize the bilirubin level in the blood, it is necessary to eliminate the underlying disease. To do this, the doctor may prescribe infusion therapy, when glucose and saline solutions, drugs, phototherapy by radiation are injected into the body, and the diet should also be changed.
“There is gallstone disease, when a stone forms in the gallbladder, – added a clinical pharmacologist. – The final stage of bilirubin release is bile. When a stone is formed, it clogged the duct, all bile begins to be absorbed back into the blood along with bilirubin, obstructive jaundice appears.If the patient is not operated on in time, the bilirubin will begin to stagnate in the bile ducts, in the future this will lead to an increase in the liver, cirrhosis will occur – the destruction of its cells. With such jaundice, doctors remove a stone or gallbladder. After the procedure, bile is not absorbed anywhere and the body begins to function normally. If we talk about infectious diseases, they are treated by infectious disease specialists, for example, all hepatitis. Patients are prescribed various drugs, including those that improve liver function. “
modern tactics and therapy strategy
O. Ya. Babak, MD, DSc, Professor, Director of the Institute of Therapy. L.T. Small AMS of Ukraine, Kharkov
Diabetes mellitus (DM) is a serious medical and social problem that attracts the attention of doctors of various specialties not only due to the high prevalence and chronic course of the disease,
but also with a large number of complications from many organs and systems, in particular the gastrointestinal tract (GIT).
The number of patients with diabetes all over the world is increasing annually. According to the WHO, by 2025 their number will reach 334 million. Thus, in the United States, 20.8 million people suffer from diabetes (7% of the population), 90,234 are registered in Ukraine.
more than 1 million patients with diabetes (about 2% of the total population), while, according to epidemiological studies, the true incidence of diabetes in our country is 2-3 times higher.
Type 2 diabetes, which is based on the development of insulin resistance (IR) and relative insulin deficiency, accounts for 90-95% of the total number of patients with this disease.According to statistics, only in the United States, a country with a high socio-economic level of development, 5.2 million people have undiagnosed type 2 diabetes. It is this pathology that is the sixth in the list of causes of death and accounts for 17.2% of deaths among people over 25 years old.
One of the causes of death associated with type 2 diabetes is liver disease. In the population study Verona Diabetes Study, cirrhosis of the liver (LC) is in 4th place among the causes of deaths of diabetes (4.4% of the number of deaths).At the same time, the standardized mortality ratio – the relative incidence of an event versus the incidence in the general population – for CP was 2.52 versus 1.34 for cardiovascular diseases (CVD). If the patient receives insulin therapy, this figure rises to 6.84. In another prospective cohort study, the incidence of LC as a cause of death in patients with diabetes mellitus was 12.5%.
According to the latest estimates, liver damage is one of the most common pathologies in diabetes.Cryptogenic LC, including that caused by diabetes, has become the third leading indication for liver transplantation in developed countries.
The development of diabetes negatively affects the state of the liver, disrupting the metabolism of proteins, amino acids, fats and other substances in hepatocytes, which, in turn, predisposes to the development of chronic liver diseases.
The pathogenesis of diabetes is based on three endocrine defects: impaired insulin production, IR, and impaired liver response to insulin, which does not lead to inhibition of gluconeogenesis.
Blood glucose is measured on an empty stomach and after meals. The liver produces glucose both through the breakdown of glycogen (glycogenolysis) and through its synthesis (gluconeogenesis). Normally, in a fasting state, a balance is maintained between the production of glucose by the liver and its utilization by the muscles. After eating, in response to an increase in blood glucose, the concentration of insulin increases. Normally, insulin stimulates the formation of glycogen in the liver and inhibits gluconeogenesis and glycogenolysis. When the liver is resistant to the action of insulin, metabolic processes are switched: the synthesis and secretion of glucose into the blood increases, the breakdown of glycogen begins, and its formation and accumulation in the liver is inhibited.With IR in skeletal muscles, the supply of glucose and its utilization by the cell are disrupted. The absorption of glucose by insulin-dependent tissues is carried out with the participation of GLUT-4.
On the other hand, under conditions of IR, a significant amount of non-esterified fatty acids (NEFA) is released into the bloodstream, namely, into the portal vein. Through the portal vein, excess NEFA enters the liver by the shortest route, where they must be utilized. One way of utilizing NEFA is their transformation into glucose through gluconeogenesis processes.Another way of utilization of NEFA entering the liver is the synthesis of triglycerides.
For many years, various terminology was used to define liver damage in diabetes, which included such concepts as “diabetic hepatopathy”, “fatty hepatosis”, “fatty liver degeneration”. However, in recent years, due to an improved understanding of the mechanisms of formation and progression of changes in the liver in diabetes, the term “non-alcoholic fatty liver disease” has become competent, combining the concepts of “non-alcoholic steatosis” and “non-alcoholic steatohepatitis”, which have common features with IR syndrome and reflect the stages of development pathological process.
In patients with type 2 diabetes, an almost full spectrum of liver diseases is observed, including abnormalities of liver enzymes, non-alcoholic fatty liver disease (NAFLD), LC, hepatocellular carcinoma (HCC), and acute liver failure. In addition, the association of type 1 and 2 diabetes with viral hepatitis C.
Liver enzyme abnormalities
norms (VGN).At the same time, initial concomitant liver pathology was diagnosed in 5% of patients. H.E. Lebovitz et al., Analyzing the results of 5003 patients with type 2 diabetes (individuals with elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), or alkaline phosphatase, exceeding ULN by> 2.5 times, were excluded from the study), revealed 5.6 % of patients with serum ALT levels from 1 to 2.5 VGN. In-depth examination of individuals with asymptomatic moderate elevations in ALT and AST revealed the presence of liver disease in 98% of patients.Most often, this clinical situation was due to fatty liver disease or chronic hepatitis.
Non-alcoholic fatty liver disease
NAFLD is one of the most common chronic liver diseases in European countries and the United States, which involves the presence of fatty liver disease without a history of alcohol abuse (<20 g alcohol / day). NAFLD has histological features of alcoholic liver disease and includes a spectrum of liver diseases ranging from steatosis (fatty infiltration of the liver without inflammation) to non-alcoholic steatohepatitis (NASH), characterized by inflammation, necrosis, and fibrosis of the liver against a background of overfilling of hepatocytes with fat.The incidence of NAFLD in diabetes varies from 34 to 74%, and when diabetes is combined with obesity, it reaches 100%. If NASH was previously considered as a benign process, then in the course of recent studies it was established that this disease leads to LC, and in some cases - to the development of HCC. Among NAFLD patients at the time of diagnosis, 50% have NASH, 19% have LC.
The pathogenesis of NAFLD in diabetes mellitus remains a matter of debate. Liver steatosis reflects an imbalance between the uptake and synthesis of fatty acids by the liver, their oxidation and excretion.In patients with type 2 diabetes, dyslipidemia is observed, characterized by an increase in plasma triglycerides, a decrease in high-density lipoprotein (HDL) cholesterol, and a prevalence of small low-density lipoprotein (LDL) subfractions. This phenomenon is also observed in patients with NAFLD without diabetes mellitus. The central link in the pathogenesis of hepatic steatosis is IR, which leads to lipolysis, which increases the level of circulating free fatty acids, which are taken up by the liver as an energy source.Fatty acids overload the system
β-oxidation in the mitochondria of hepatocytes, leading to the accumulation of fatty acids in the liver.
The course of NAFLD resembles the course of alcoholic liver disease. The progression of the process from steatosis to steatohepatitis up to LC, and in some patients – HCC takes many years. The prognosis worsens with each subsequent stage of the disease. The predictors of severe NAFLD are type 2 diabetes and metabolic syndrome. Regular liver biopsy and non-invasive detection of liver fibrosis markers are the main tests for determining the prognosis of the disease.
Cirrhosis of the liver
CP is one of the causes of death associated with diabetes. According to autopsy data, the incidence of severe liver fibrosis in patients with diabetes is higher than in patients without diabetes.
The course of CP and DM is complicated by the fact that the course of CP itself is associated with the development of IR. At the same time, impaired glucose tolerance is observed in 60% of cases, and overt diabetes is observed in 20% of patients with CP. However, the manifestation of type 2 diabetes in patients with LC is more often accompanied by a decrease rather than an increase in insulin secretion.These features complicate the study of the pathogenesis of cirrhosis in diabetes and create the appropriate prerequisites for drug correction.
According to the results of numerous studies, the prevalence of HCC among people with diabetes is 4 times higher than in the general population.
The pathogenetic sequence of events leading to HCC includes IR, increased lipolysis, lipid accumulation in the hepatocyte, oxidative stress, and cell damage, followed by fibrosis and cell proliferation, which are procarcinogenic processes.
Acute liver failure
The incidence of acute liver failure in patients with diabetes is 2.31 per 10 thousand people compared to 1.44 in the general population. It is possible that drugs or other factors increase the risk of acute liver failure in this group of patients. These statistics do not include cases of acute liver failure while taking troglitazone.
The prevalence of viral hepatitis C (HCV) among patients with both type 1 and type 2 diabetes is higher compared to the general population.
For the first time, the specific association of type 2 diabetes with HCV became known in 1994, when Allison et al., Examining a cohort of patients with LC of various etiologies, found that type 2 diabetes is more common in HCV-positive individuals. Later, this fact was repeatedly confirmed. In various studies, an increased incidence of type 2 diabetes was found in patients with severe HCV-associated liver pathology compared with patients with LC of viral and non-viral genesis (62 versus 24%), as well as compared with the control group (13 and 3%, respectively) …In the largest retrospective study in the United States, which included 1117 patients with chronic viral hepatitis, the incidence of type 2 diabetes in HCV-infected patients was 21%, while among patients with viral hepatitis B (HBV) it was only 12%. The latter circumstance indicates that HCV is more likely to predispose to the development of diabetes than liver disease itself.
Patients who underwent liver transplantation for HCV developed diabetes more often than those who underwent this intervention for other liver pathologies.
Today, there is every reason to believe that HCV plays an important role in the pathogenesis of type 2 diabetes. This is confirmed by the fact that the HCV nuclear protein disrupts the insulin cascade of reactions.
Another feature of HCV in diabetes is the specificity of the genotype of the virus. An association was noted between HCV genotype 3 infection and the development of hepatic steatosis in diabetes mellitus. It has been shown that in patients with HCV, especially those infected with genotype 3 of the virus, and fatty liver disease, the level of TNF-α is increased and adiponectin is decreased, which promotes inflammation and steatosis of the liver, initiates the development of oxidative stress in the mitochondria of hepatocytes and the “overflow” of cells with fat.
In recent years, interesting data have been obtained on the existence of a relationship between diabetes mellitus and treatment of HCV infection with interferon-α. It was shown that type 1 diabetes occurred more often in patients who were treated with interferon for HCV. The period of latent diabetes mellitus ranges from 10 days to 4 years after the start of treatment. The interaction between HCV infection, diabetes mellitus and interferon is currently the subject of intense research.
Based on the epidemiological data on the widespread prevalence of HCV among people with diabetes, it is reasonable to screen all patients with diabetes and elevated ALT levels for the presence of HCV.
Management of patients with liver diseases
and type 2 diabetes
Based on the fact that at least 50% of patients with type 2 diabetes have NAFLD, ALT and AST tests should be performed in all patients.
A diagnosis of NAFLD or NASH should be suspected in every patient with type 2 diabetes, especially if abnormal liver function tests are found. Particular attention should be paid to patients with type 2 diabetes with increased body weight. Usually ALT is 2-3 times higher than ULN, but it can remain normal.Moderate increases in alkaline phosphatase and glutamyl transferase levels are often observed. Serum ferritin levels are often elevated, while iron levels and iron-binding capacity remain normal.
95% of patients with diabetes, regardless of the degree of elevation of ALT and AST, have chronic liver disease. The most common causes of mild elevations in ALT / AST are NAFLD, HCV, HBV, and alcohol abuse. Moderate alcohol consumption (<20 g / day) does not increase liver enzyme levels.
Initial screening should include identification of HCV markers (anti-HCV, HCV-RNA), HBV (HBsAg, anti-HBV, HBV-DNA), hemochromatosis (iron and iron saturation) and ultrasound (ultrasound) of the abdominal organs. The predictor value of abdominal ultrasound for detecting NAFLD in the absence of other pathology is 96%. Ultrasound can reveal a diffuse increase in liver echogenicity. The sensitivity of ultrasound in patients with elevated ALT levels is 89%, the specificity is 93%.Magnetic resonance spectroscopy can quantitatively confirm the presence of steatosis, but is not indicated for use in routine clinical practice. Puncture biopsy of the liver remains the standard for the diagnosis of NAFLD. Only through this method is it possible to reliably determine progressive steatohepatitis – a condition that precedes CP. The definition of AST / ALT> 1, hypertriglyceridemia and thrombocytopenia allows to identify a high-risk group for the progression of NAFLD. A diagnostic panel of serum markers of liver fibrosis is under development, which allows for long-term dynamic monitoring of the degree of fibrosis and its widespread use in clinical practice.
Treatment of NAFLD
To date, there are no treatment regimens for NAFLD, as well as FDA recommendations on the choice of drugs for this disease. Modern approaches to the treatment of this pathology are mainly aimed at eliminating or weakening the factors leading to its development. Weight loss, correction of hyperglycemia and hyperlipidemia, and elimination of potentially hepatotoxic drugs are the main principles of NAFLD therapy.
The feasibility of treatment was noted only in those patients in whom the diagnosis of NASH was confirmed by liver biopsy or who have the above risk factors.
Initiation of treatment for NASH consists of weight loss and exercise, which increases peripheral insulin sensitivity and decreases hepatic steatosis. However, rapid weight loss can increase necrosis, inflammation and fibrosis, which may be due to an increase in circulating free fatty acids due to increased lipolysis. The ideal rate of weight loss is not known; the recommended rate is 1.5 kg per week. Since saturated fatty acids increase IR, it is desirable for NAFLD patients to follow a diet high in monounsaturated fatty acids and low in carbohydrates.
To date, data from many studies demonstrate a decrease in hepatic steatosis during treatment, however, long-term trials to determine the natural course of the disease and the possibility of relapse after treatment have not yet been carried out.
Pathogenetically justified in NAFLD in the setting of diabetes is the use of thiazolidinediones (pioglitazone, rosiglitazone) – drugs that increase insulin sensitivity. This group of drugs should be considered as the drugs of choice.
Five studies have now been published using pioglitazone for 16-48 weeks, and one large multicenter placebo-controlled trial is nearing completion. All of these studies demonstrated a decrease in serum ALT levels and most of them showed an improvement in the histological picture. G. Lutchman et al. note that the use of pioglitazone, in addition to increasing the level of adiponectin, reducing glycosylated hemoglobin, increasing insulin sensitivity, improved the histological picture of the liver – reducing steatosis, inflammatory changes and liver fibrosis.
Prescribing rosiglitazone to patients with NAFLD with diabetes for 24 weeks also improves the histological picture of the liver. A significant decrease in the levels of ALT, AST, gamma-glutamyl transpeptidase and an improvement in insulin sensitivity are noted with the use of rosiglitazone at a dose of 8 mg / day for 48 weeks.
Regarding the use of biguanides (metformin), it is known that their appointment leads to a decrease in ALT, while the histological picture does not change.
Cytoprotective therapy for NAFLD and DM is carried out using ursodeoxycholic acid (UDCA) and essential phospholipids (EF). The effectiveness of UDCA has been demonstrated in three prospective controlled studies, during which its effect on reducing the severity of apoptosis was shown. The ability of EF to provide antioxidant, anti-fibrotic and anti-inflammatory effects makes it possible to recommend these drugs to patients with NAFLD.
Treatment of viral hepatitis C
Most effective HCV treatment regimens are based on a combination of pegylated interferons and ribavirin.The effect of interferon on insulin sensitivity and glucose tolerance has been proven. Taking into account the possible unpredictable effects of interferon on the course of diabetes, during this type of treatment, it is necessary to extremely carefully monitor the level of glycemia.
Of interest are the results of recently published trials indicating a hepatoprotective role for statins in HCV infections.
In their practice, doctors do not always think about the side effects that hypoglycemic drugs can have.When prescribing treatment for a patient with diabetes mellitus with liver disease, one should remember about possible metabolic disorders of drugs, the interaction between them and hepatotoxicity. Metabolic disorders of drugs are usually observed in patients with a history of liver failure, ascites, coagulopathy, or encephalopathy.
Although metformin is used as the first-line drug for most patients, it is not recommended for patients with severe liver damage due to an increased risk of lactic acidosis.
Taking into account the experience of using troglitazone, which has been removed from the pharmaceutical market, the question of the possible hepatotoxicity of thiazolidinediones remains the subject of in-depth study. In clinical trials using rosiglitazone and pioglitazone, a threefold increase in ALT levels was observed with the same frequency as in the case of using rosiglitazone (0.26%), pioglitazone (0.2%) and placebo (0.2 and 0.25%) … At the same time, when using rosiglitazone and pioglitazone, a significantly lower risk of developing acute liver failure was noted than when taking troglitazone.The FDA has received 68 cases of hepatitis and acute liver failure due to rosiglitazone treatment and 37 cases from pioglitazone therapy. However, a causal relationship with the use of these drugs was not confirmed, since the situation was complicated by concomitant drug treatment and cardiovascular pathology.
In this regard, it is recommended to assess the level of ALT before starting treatment with rosiglitazone and pioglitazone. Treatment should not be initiated if active liver disease is suspected or if ALT levels are more than 2.5 times the ULN.Subsequently, it is advisable to monitor liver enzymes every 2 months.
Sulfonylureas that stimulate insulin secretion are generally safe for patients with liver disease, but do not affect IR. In patients with decompensated LC, that is, the presence of hepatic encephalopathy, ascites, or coagulopathy, the appointment of these drugs is not always effective in achieving normoglycemia. Chlorpropamide leads to the development of hepatitis and jaundice. Treatment with repaglinide and nateglinide is not associated with the development of hepatotoxicity.
A-glycosidase inhibitors are safe for patients with liver diseases, since they directly affect the gastrointestinal tract, reduce carbohydrate absorption and postprandial hyperglycemia. Moreover, acarbose has been shown to be effective in the treatment of patients with hepatic encephalopathy and type 2 diabetes.
When carrying out insulin therapy in patients with decompensated liver disease, the dose of insulin may be reduced due to a decrease in the intensity of gluconeogenesis and insulin metabolism.At the same time, patients with impaired liver function may have an increased need for insulin due to the presence of IR, which requires careful monitoring of glycemic levels and frequent dose adjustments.
Fast-acting insulin analogues can be used to treat patients with hepatic encephalopathy requiring a high-carbohydrate diet that promotes postprandial hyperglycemia.
Summing up, it should be noted that diabetes mellitus is associated with a wide range of liver diseases, including increased liver enzymes, fatty liver disease, LC, HCC, and acute liver failure.There is a definite connection between the presence of diabetes and HCV. Many researchers view NAFLD as part of the IR syndrome. Ideal treatment regimens for NAFLD in patients with diabetes, as well as in combination with diabetes mellitus with liver pathology, have not yet been developed; there are also no recommendations based on the principles of evidence-based medicine regarding the tactics of managing such patients. In this regard, in everyday practice, the doctor, first of all, must focus on the underlying cause of the disease. The study of the mutual influence of two pathological conditions – chronic inflammatory process in the liver and relative or absolute insulin deficiency – is a promising area of modern medicine.
References are being revised.
Oncology and hematology
Lykar-oncologist about the difficult specialties of diagnostics of oncological illnesses
Cancer – tse zhvoryuvannya, like current medicine in diagnostics, lіkuvati and control.The emergence of ailments at an early stage allows one to recognize a type of therapy, and at the same time, when we are happy with it. The very fact is timely diagnostics of the vital role in the successful detection of oncological illnesses. About the specialties of diagnostics of oncological pathology of the development of the leader directly oncology, surgeon-oncologist of the Dobrobut medical hedgehog Kostyantin Volodimirovich Kopchak ….
Pachydermodactylia is an unseen diagnosis in the case of the suglobovy syndrome
Speak, if the patient has a symmetrical increase in the diameter of the midphalangeal lobes of the hands, the diagnosis of arthritis is most often established. Allegedly, there are some symptoms, not associated with ignition processes in cich troughs.Pahіdermodaktiliya (from the walnut pachy – tovsty, dermos – shkіra, dactylos – fingers) – one of them, children develop a little, so don’t expect the right diagnosis …
Donate blood for Alanine aminotransferase (ALAT) in Zaporozhye in MC “SHEKI”
Alanine aminotransferase (ALT) is an enzyme belonging to the class of transferases.It participates in the formation of glutamate and pyruvic acid. ALTs are found in organs such as the kidneys, heart, pancreas, skeletal muscles, but mostly in the liver. Intracellular metabolism can be disrupted due to infectious or toxic effects on it, which leads to a violation of the permeability of the cell membranes. This entails cytolysis – the ingress of cytoplasmic components into the blood serum, thereby provoking an increase in the activity of ALT in the blood. Under normal conditions, a small amount of the enzyme enters the bloodstream.An increase in this indicator indicates the presence of a cytolytic sidrome, but does not indicate the degree of organ damage. Therefore, it is advisable to consider the ALT indicator in dynamics. It is ALT that makes it possible to determine abnormalities in the liver – hepatitis, two weeks before the first symptoms appear. This is especially true for acute hepatitis A. Three weeks after infection with hepatitis A, the ALT indicator returns to normal. Hepatitis B and C give unpredictable fluctuations in ALT. You can donate blood for ALAT in Zaporozhye at the “SHEKI” medical center.The center’s laboratory has been helping doctors diagnose diseases for more than ten years and has established itself as a reliable partner. Analyzes are always performed quickly and with a guarantee of high accuracy of the result. For research, venous blood is donated on an empty stomach. The result is ready within a day.
Who is assigned an ALT test?
Alanine aminotransferase is one of the most important indicators of cytolysis in the presence of liver disease. Who do doctors recommend to take the test for ALT ? To everyone who:
• Has complaints of pain in the right hypochondrium, enlarged liver, bitterness in the mouth, yellowing of the skin and other signs of liver dysfunction
• When making a diagnosis of diseases of the pancreas and biliary tract
• To monitor the treatment of liver diseases – viral hepatitis
• To clarify the diagnosis
• Planning pregnancy
• If you wish to become a blood donor
• For planned surgery
• When carrying out preventive examinations, if there were violations of the gastrointestinal tract
In order for the result of the study to be as accurate as possible, it is necessary to properly prepare for the delivery of the analysis.
When can the alanine aminotransferase rate be increased?
An increase in the enzyme can also be observed in a number of cases when there is no inflammatory or toxic damage to cells:
• When taking medications – vorfarin, paracetamol, aspirin, oral contraceptives. Also, drugs based on the herb valerian and echinacea increase ALT levels.
• In the first trimester of pregnancy (a slight increase is considered normal)
• With significant physical activity before taking the test
• In case of power failure before taking the test
What does the increase in the Alanine aminotransferase index indicate?
Deviations from normal values by more than five times may indicate problems such as:
• Liver cirrhosis
• Oncological processes in the liver
• Myocardial infarction
Conducting competent therapy allows to reduce the ALT indicator to normal values.An important role in this is played by adherence to the correct diet, dosed physical activity, normalization of the patient’s weight and psychoemotional state, as well as monitoring the ALT indicator in dynamics.
Phosphatase alkaline total – To pass the analysis in Rostov-on-Don
Diseases of the liver and biliary tract are diagnosed using a set of laboratory tests. One of them is the analysis for total alkaline phosphatase – if the content of this substance in the blood rises sharply, this indicates the death of liver cells and a violation of the normal outflow of bile.Its congestion is also caused by the accumulation of stones in the bile ducts. In addition, this analysis can be prescribed to detect bone diseases, rapid growth of a malignant tumor.
What is total alkaline phosphatase?
Total alkaline phosphatase is an enzyme found in the tissues of the liver and bile ducts. It is used as an important component of biochemical reactions and does not work when it enters the bloodstream. The liver cells are gradually changing, so a small amount of the enzyme is constantly present in the bloodstream.However, if it becomes too much, this indicates a disease with the death of a large number of liver cells. Also, an increase in alkaline phosphatase often indicates a malfunction of the biliary tract, pathologies of bone tissue (osteosarcoma, osteoporosis). During pregnancy, the normal activity of alkaline phosphatase is increased, since it is contained in the placenta. A temporary increase in alkaline phosphatase activity is observed after fractures. In children and young men, activity is active. ALP is higher than in adults, so bone growth occurs in them.
Possible analysis results:
The norm of total alkaline phosphatase is 35-105 U / L for women and 40-130 U / L for men, for children the normal values are different.
The total alkaline phosphatase is reduced. The reasons are anemia, dysfunction of the thyroid gland, lack of magnesium in metabolism.
Increased enzyme levels.Common causes are disorders of the liver and biliary tract (cancer, cirrhosis, hepatitis, accumulation of stones in the bile ducts). Also, the reasons can be osteosarcoma and other tumor processes of bone tissue, pathological growth.
To conduct a blood test for alkaline phosphatase, the following preparation requirements must be met:
Quit smoking at least half an hour before receiving a blood test.
Do not eat for at least 12 hours prior to testing.
Avoid physical and emotional stress for at least half an hour before the study.
When is the test scheduled?
Determination of deviations from the norm of alkaline phosphatase is required for the diagnosis of liver diseases, the detection of tumor processes in the liver and bone tissue, and the diagnosis of gallstone disease.In addition, this study is included in the list of “liver tests”, which are prescribed for general examinations.
Where to conduct research in Rostov-on-Don?
Clinical and Diagnostic Center “Da Vinci” conducts inexpensive laboratory tests to identify pathologies of the liver and other internal organs. High accuracy of examination results is guaranteed.
Liver fibrosis – treatment of the disease, prognosis
Liver fibrosis (AF) is the process of replacing organ tissue with connective tissue, which is
the body’s universal response to damage. 1 Liver fibrosis is dangerous because it is
impairs liver function, and if diagnosed late, one of the outcomes of fibrosis can be
Mechanism of development of fibrosis
Fibrosis develops in response to various damaging actions: viral, toxic, metabolic
violations and others. Fibrosis is the result of damage to the liver tissue and is accompanied by
activation of stellate cells with their subsequent production of collagen, which, in general,
and is a connective tissue.If the balance between fibrosis and processes
recovery is preserved, then under the action of the collagenase enzyme, the process of lysis (destruction) of an excess amount of connective tissue occurs. With chronic liver damage, regeneration processes
in the liver are violated, and fibrosis progresses 1 . With fibrosis, it can be observed like this
“Shunting” of blood, that is, the blood entering the liver goes directly to the hepatic
veins without contacting properly with hepatocytes.Without this contact, the liver is naturally more difficult
fulfill their functions.
Fibrosis is generally considered a nearly irreversible condition, although in recent experimental
research and in some diseases, in the case of successful treatment, it is possible to some
degree to achieve its regression 1.2 . These developments are encouraging and hopeful
medicine of the future will confidently cope with even this problem.
Causes of fibrosis
As already mentioned, chronic inflammation in hepatocytes leads to fibrosis,
which in turn can be caused by 1.5 :
- Viral hepatitis (B, C, D)
- Epstein-Barr virus
- Cytomegalovirus infection
- Toxic effects of alcohol
- Autoimmune disorders
- Fat and carbohydrate metabolism disorders
- Congenital diseases, including storage diseases
- Toxic effects of certain drugs
- Primary sclerosing cholangitis and other diseases
However, one of the most common causes of liver fibrosis is considered non-alcoholic fatty disease.
liver, which is affected according to a large-scale multicenter domestic study
DIREG2 37% of the adult population of the Russian Federation 6 , that is, almost every third adult
in the country.Its occurrence is associated with a violation of the metabolism of fats and carbohydrates, the presence
overweight or obesity, as well as type 2 diabetes mellitus, in particular lying
it is based on insulin resistance – a decrease in the sensitivity of the receptor apparatus of cells
and tissues to insulin 6 The disease begins with the stage of steatosis – so
called “fatty liver”. Subsequently to fatty degeneration of the liver, that is
steatosis, inflammation joins, which further leads to the replacement of hepatocytes
connective tissue and the formation of fibrosis. 6
Forms of fibrosis
There are several types of fibrosis, for example, perisinusoidal fibrosis is distinguished – growth
fibrous tissue in the perisinusoidal space of Disse (the space between the sinusoidal capillaries
and hepatocytes). In this case, liver cells are quickly isolated from the bloodstream. Install
the form of fibrosis is possible only on the basis of biopsy results.
Stages of the disease
According to the results of a biopsy (histological examination of liver tissue under a microscope), the
the severity of fibrosis.
To do this, use the scale for assessing the severity of liver fibrosis – system
Metavir 5 :
Expansion of portal paths, but without
Expansion of portal paths
with single port – portal septa
Port-portal and port-central
However, this diagnostic method has a number of disadvantages 5 : it is an invasive method,
to each patient with liver fibrosis.Moreover, biopsy is associated with
with a high risk of complications from bleeding to accidental damage to neighboring organs,
such as the gallbladder, etc.
What methods of diagnosing fibrosis can be used in almost every patient?
It should be noted that since the liver tissue does not have nerve endings, “the liver
does not hurt”. Pain occurs only when the organ is significantly enlarged and the capsule is stretched
liver.If we are talking about fatty liver disease as the cause of fibrosis, then at the initial
stages of the disease, namely at the stages of steatosis and steatohepatitis, specific complaints,
indicating the development of the disease may be absent.
The patient may complain about:
emerging weakness, fatigue
discomfort in the right hypochondrium
nausea, impaired appetite 6
Yellowing of the skin and mucous membranes, the appearance of spider veins on the skin
(telangiectasia), the occurrence of ascites (free fluid in the abdominal cavity) is most often indicated
on the onset of cirrhosis – a condition that is irreversible, for the treatment of which, as
usually a liver transplant is required.
In the diagnosis of liver fibrosis, the results of laboratory tests are used.
There are so-called liver fibrosis markers, which are divided into:
Reflect the dynamics of the number of fibrous fibers and changes
Indicate violations of hepatic function.These include enzymes AST, ALT, bilirubin,
moreover, an increase in the activity of the AST enzyme is more associated with the development of fibrosis than
Evaluation of the results of studies of indirect markers in the aggregate increases their diagnostic
value. This is the basis for the use in clinical practice of such diagnostic panels as
FibroTest, FibroMax, etc. The diagnostic accuracy is
from 70 to 100% 1 , which makes it possible to a certain extent to consider
these diagnostic panels for assessing the severity of fibrosis as non-invasive analogs of biopsy6.
Liver tissue imaging methods such as ultrasound, CT and MRI are also quite useful.
With their help, the size, shape, structure of the organ, as well as the state of
blood flow 1.6 .
Ultrasound diagnostic methods also include liver elastometry, which is performed
using the FibroScan 1 and allows you to judge the elasticity of the liver tissue
at various sites.
Timely diagnostics, allowing to assess the severity of fibrosis, allows you to prescribe optimal therapy
and improve the prognosis of the disease.
Treatment of liver fibrosis
As we already understood, fibrosis is a common consequence of various diseases, and therefore it is not fibrosis that needs to be treated, but
the pathology that caused it.
To the main areas of therapy for liver diseases that can lead to fibrosis,
refer 3 :
- Elimination of the effect of the damaging factor
- Cessation of alcohol for alcoholic liver disease
- Cancellation of drugs with toxic effects on hepatocytes
with drug damage to the liver 90 128
- Change in lifestyle, adequate physical activity, weight loss
and normalization of carbohydrate and fat metabolism in the case of fatty hepatosis 90 128
- Specialized antiviral therapy for viral hepatitis for
elimination of viral particles that damage liver cells
In general, drug therapy includes those drugs that are relevant for a specific
the disease that caused fibrosis.If there is a specialized medicinal product for viral hepatitis
therapy, then with alcoholic liver disease it is not. It has been shown that no remedy
does not prolong the life of the patient except for refusing alcohol. Any medications can be taken
and deluding oneself by “swallowing the medicine and maintaining the liver after alcohol”,
but this does not affect the forecast in any way. The main thing with this pathology is to take a firm
the decision to stop taking alcoholic beverages.With fatty hepatosis of non-alcoholic origin
it is incredibly important to change your lifestyle, go in for sports. At the same time, there are also medicinal
drugs that reduce the “fat load” (steatosis) in the liver 9 . These are drugs
essential phospholipids, which not only help repair liver cells by protecting
them from toxic effects, but also help slow down the progression
Biochemical blood test – decoding of biochemistry
A biochemical blood test has to be taken almost more often than a general clinical one.We will help you understand the main indicators of “biochemistry”.
Doctor on duty online consultation service Doctis will help you to decipher your blood test free of charge . Download the mobile app.
Glucose. The norm is 3.9-5.8 mmol / l
An increase in fasting glucose in the results of a biochemical blood test indicates a violation of carbohydrate metabolism in varying degrees of severity – from impaired glucose tolerance to type 1 or 2 diabetes mellitus.The upper limit of the norm is declared as 5.8 mmol / l, but recently many experts “push” this limit to 6.1 mmol / l for people over 60 years old.
Indicators in the corridor from 6.1 to 6.69 indicate a violation of glucose tolerance or prediabetes, at this stage it is not too late to stop the development of the disease by changing the diet, losing weight and getting rid of bad habits.
A reading above 6.7 mmol / L most likely indicates diabetes, but this is not final.Endocrinologists advise in this case to take an additional test for glycated hemoglobin – it will demonstrate the average blood plasma glucose over the last three months.
ALT. The norm is less than 31 U / L for women and 41 U / L for men.
This enzyme is synthesized mainly in the liver, and usually only a small amount will enter the bloodstream. An increase in the values in the analysis results is characteristic of liver diseases – fatty hepatosis, (when, due to malnutrition with a predominance of fatty foods and alcohol, hepatocytes are replaced by fat cells), as well as hepatitis – viral, toxic (where alcohol comes first, then medicinal), autoimmune and others, as well as liver cirrhosis.Another possible reason for the increase is a recent myocardial infarction.
AST. The norm is less than 31 U / L for women and 37 U / L for men.
Also a hepatic enzyme, an increase in the concentration in the blood indicates the defeat of this important organ. True, it is also found in the heart, kidneys, skeletal muscles. It rarely rises in isolation and almost always accompanies an increase in ALT. In this case, you need to immediately contact a gastroenterologist, the liver suffers. In isolation, it can increase with myocardial infarction, kidney injury, damage to skeletal muscles, heart failure.And sometimes – and after excessive physical exertion.
GGTP. The norm is less than 49 U / L for women and 32 U / L for men.
Another “hepatic” indicator and the main marker of cholestasis is stagnation of bile. And its increase often indicates the frequent abuse of alcoholic beverages.
Total bilirubin. The norm is 3.4-17.1 μmol / l.
An important indicator of liver function, the main component of bile. If the value is normal, then all links are working properly. If the indicator in the results of the biochemical blood test is increased, the laboratory will conduct an additional analysis and find out due to which component the increase occurred.There are two of them – direct (bound) and indirect (free) bilirubin . If the increase was due to the indirect, then the problem is in the release of bilirubin from the blood cells, hemolysis occurs in the body – the destruction of red blood cells. If due to direct, then there is a problem in the liver, a violation of the secretion and absorption of bile begins or is already taking place, clinically manifested by jaundice.
Amylase. The norm is 28-100 U / l.
Pancreatic enzyme, which is also found in the intestines.An increase in amylase in the biochemical parameters of the blood indicates the development of pancreatic inflammation – acute or chronic pancreatitis. If bowel damage cannot be ruled out, a more targeted test for pancreatic amylase should be performed.
Total protein. The norm is 64-83 g / l.
Indicator of basal protein metabolism in our body. Possible – hypoproteinemia (decrease in the level), hyperproteinemia (increase in the level) and dysproteinemia (violation of the ratio of the main proteins – albumin and globulins).An increase in the level of protein in a biochemical blood test indicates a rich diet rich in protein. A decrease in levels is a dangerous symptom that can speak of many reasons, ranging from starvation to cancer.
Total cholesterol. The norm is 3.0-7.2 mmol / l, depending on gender and age.
Indicator of the level of total cholesterol currently contained in plasma. An increase in the level is traditionally considered an unfavorable sign of the development of vascular atherosclerosis, although in fact, clarification is required due to which component the increase occurs.(We will tell you separately about “bad and” good “cholesterol in the nearest future).
Creatinine. The norm is 53-97 μmol / L for women and 62-115 μmol / L for men.
Indicator of the urinary system. An increase in the level of creatinine in the results of biochemical analysis indicates a particular stage of renal failure. But it can also increase in blood after significant physical exertion, temporary “overload” of the kidneys with protein foods or drugs, in athletes. Such an increase will normalize after a while.
Urea. The norm is 2.5-6.4 mmol / l, after 60 years – 2.9-7.5 mmol / l.
Another “renal” indicator. In fact, this is an indicator of the level of protein breakdown, but usually an increase in urea levels does not indicate this, but rather the inability of the kidneys to excrete the usual amount of breakdown protein.
Doctors use this biochemical blood test to monitor the treatment of renal failure and assess the condition of patients. Protein diets may occasionally increase urea levels with relatively healthy kidneys.
Uric acid. The norm is 150-350 μmol / L for women and 210-420 μmol / L for men.
Despite the name, it is no longer used to assess the condition of the kidneys, but to identify gout. It is about the development of this disease that the increase in uric acid in the plasma speaks, and the appearance of joint pain typical for the disease only confirms the laboratory diagnosis.
Potassium. The norm is 3.5-5.5 mmol / l.
An increase in the level of this electrolyte most often indicates the development of renal failure, as a result of which the excretion of electrolyte is impaired.Potassium above 6.5 mmol / l is dangerous for possible cardiac arrest. A decrease in the level is caused by a large loss of fluid (vomiting, diarrhea, often profuse urination) and is fraught with the development of cardiac arrhythmias (atrial fibrillation).
Sodium. The norm is 136-145 mmol / l.
A decrease in the level is associated with dehydration, an increase with impaired renal function, but not as pronounced as in the case of potassium. A decrease in sodium concentration in the results of biochemical analysis is manifested by general weakness and various neurological disorders, an increase is often combined with an increase in blood pressure.
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