what is the reason of high SGPT enzyme in liver? and what is the treatment or medicine of this?
928242
Serum glutamic pyruvate transaminase is an enzyme in liver cells that facilitates creation of pyruvate as a source of energy in temporarily dysfunctional liver cells. Thus SGPT is elevated in infective  hepatitis. After the liver cells recover spontaneously from infection SGPT levels become normal. There is no medicine to reduce SGPT levels. SGPT elevation is a result not a cause of liver disease.
424403
A liver enzyme is a protein that helps to speed up a chemical reaction in the liver. Liver function tests are blood tests that are used to evaluate various functions of the liver - for example, metabolism, storage, filtration and excretion, which are often performed by liver enzymes. However, not all liver function tests are measures of enzyme function. \n\nDescription\n\nThe liver is an important internal organ because it performs many functions. It helps detoxify the many toxins in the body, makes proteins that are used to help clot the blood (clotting factors) and other proteins that help draw fluid into our blood vessels (e.g., albumin). Liver function tests are blood tests that include alkaline phosphatase, prothrombin time (PT, a measure of blood clotting), serum bilirubin and serum albumin. The most commonly used indicators of liver damage are the alanine aminotransferase (ALT) and aspartate aminotransferase (AST), formally referred to as SPGT and SGOT. These are enzymes normally found in liver cells that leak out of these cells and make their way to the blood when liver cells are injured. The ALT is felt to be a more specific indicator of liver inflammation, as AST is also found in other organs, such as the heart and skeletal muscle. In acute injury to the liver, as in viral hepatitis, the level of the ALT and AST may be used as a general measure of the degree of liver inflammation or damage. In chronic liver disease, this is not the case, for these enzymes may be entirely within the normal range, even in the presence of cirrhosis (scarring of the liver). Increased levels of ALT and AST can have a large number of clinical implications. Elevated levels might involve hepatocellular disease, active cirrhosis, metastatic liver tumor, infection or toxic hepatitis, severe burns, pancreatitis, myocardial infarction (heart attack), trauma, severe burns, acute hemolytic anemia, crushing injuries, gangrene or shock. Alkaline phosphatase is the most frequently used test to detect obstruction in the biliary system. Elevation of this enzyme may be found in a large number of disorders as common as gallstone disease, alcohol abuse and drug-induced hepatitis, or in less common disorders, such as primary biliary cirrhosis or biliary tumors. Although this enzyme is found both in the liver and the bile, it leaks into the bloodstream in a manner similar to that of the ALT and AST. Alkaline phosphatase is also found in other organs, such as bone, placenta and intestine. Prothrombin time (PT) is a one measure of blood clotting. It may be elevated when there is damage to the liver, meaning that there is a greater tendency to bleed. PT is also used to monitor the appropriate dose of coumadin (warfarin) for certain patients who need blood-thinners (anti-coagulation). Low serum albumin may cause blood vessels to be leaky and allow fluid to accumulate in the abdomen (ascites) or elsewhere in the body. Serum bilirubin is usually elevated in patients with jaundice.
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Corn Syrup and other corn yes check the site out below I'm glad you brought this question up actually I have liver problems and I never had a clue that corn was bad for you\n\nFor many years, Dr. Meira Fields and her coworkers at the US Department of Agriculture investigated the harmful effects of dietary sugar on rats. They discovered that when male rats are fed a diet deficient in copper, with sucrose as the carbohydrate, they develop severe pathologies of vital organs. Liver, heart and testes exhibit extreme swelling, while the pancreas atrophies, invariably leading to death of the rats before maturity.\n\nSucrose is a disaccharide composed of 50 percent glucose and 50 percent fructose. Dr. Fields repeated her experiments to determine whether it was the glucose or fructose moiety that caused the harmful effects. Starch breaks down into glucose when digested. On a copper-deficient diet, the male rats showed some signs of copper deficiency, but not the gross abnormalities of vital organs that occur in rats on the sucrose diet. When the rats were fed fructose, the fatal organ abnormalities occured. \n\nLysl oxidase is a copper-dependent enzyme that participates in the formation of collagen and elastin. Fructose seems to interfere with copper metabolism to such an extent that collagen and elastin cannot form in growing animals—hence the hypertrophy of the heart and liver in young males. The females did not develop these abnormalities, but they resorbed their litters.1\n\nThese experiements should give us pause when we consider the great increase in the use of high fructose corn syrup during the past 30 years, particularly in soft drinks, fruit juices and other beverages aimed at growing children, children increasingly likely to be copper deficient as modern parents no longer serve liver to their families. (Liver is by far the best source of copper in human diets.) \n\n“The bodies of the children I see today are mush,” observed a concerned chiropractor recently. The culprit is the modern diet, high in fructose and low in copper-containing foods, resulting in inadequate formation of elastin and collagen—the sinews that hold the body together.
1175040
A normal SGOT level in 8-20 u/L, so yes it is a bit high.  Possible causes might include liver disease, a heart attack, muscle trauma, pancreatitis, OD on narcotics, brain damage, kidney failure, or recent surgery or a cardiac catheterization.
1025904
Liver enlargement is also known as Hepatosplenomegaly. \n\nWhat is it?  \n\nHepatomegaly is the enlargement of the liver beyond its normal size. Hepatosplenomegaly is enlargement of both the liver and the spleen \n\nHow does the liver enlarge? \n\nThe body's immune response against the infected liver cells (hepatocytes) damages the cells, causing liver inflammation. As a result, liver enzymes (transaminases) leak out of the liver into the blood, causing transaminase blood levels to be elevated. \n\nHow do you come to know about it?\n\nThe lower edge of the liver normally comes just to the lower edge of the ribs (costal margin) on the right side. In its normal state, the edge of the liver is thin and firm, and it cannot be palpated (felt with the finger tips) below the edge of the costal margin.\n\nIf the liver becomes enlarged enough that it can be palpated below the costal margin, the patient may have hepatomegaly. The diagnosis must be confirmed by an imaging study of the liver.\n\nThe liver is involved in many bodily functions, and is affected by a variety of conditions, many of which result in hepatomegaly. General causes include infection (viral, bacterial, or parasitic), malignancy (cancer or tumors), anemias, storage diseases, heart failure, congenital heart disease, toxins, and metabolic disturbances.\n\nCommon Causes    \n\nAlcohol \nHepatitis A \nHepatitis B \nCongestive heart failure \nInfectious mononucleosis \nLeukemia \nTumor metastases \nNeuroblastoma \nHepatocellular carcinoma \nNiemann-Pick disease \nHereditary fructose intolerance \nGlycogen storage disease \nPrimary biliary cirrhosis \nSarcoidosis \nSclerosing cholangitis \nHemolytic-uremic syndrome (HUS) \nReye's syndrome
190080
Treatment    Return to top \n\nTreatment for this disease concentrates on avoiding low blood sugar. Frequent feedings are needed during the day, especially foods that contain carbohydrates (starches). Neither fruit nor milk sugar can be adequately broken down in this disease, and are best avoided.\n\nOvernight fasting is avoided by continuous feedings (through a tube that goes through the nose into the stomach) of sugars or uncooked cornstarch. The tube can be put in at bedtime and taken out each morning. A medication called allopurinol, which can lower blood uric acid and decrease the risk for gout, is often used.\n\nSynonyms:\nvon Gierkes disease\nGlucose-6-Phosphatase Deficiency Glycogen Storage Disease\nType I Glycogenosis\nHepatorenal Glycogenosis\n\nIn Type I Glycogen Storage Disease, the enzyme glucose-6-phosphatase is defective in the liver, kidney, and small intestine, where it normally functions. However, the metabolic problem is centered in the liver.\n\nPatients with Type I GSD are unable to release glucose from glycogen. They cannot maintain their blood glucose levels and within a few hours after eating develop hypoglycemia (low blood sugar). The low levels of glucose in the blood of these patients often result in chronic hunger, fatigue, and irritability that is especially noticeable in infants. Symptoms of hypoglycemia only begin to appear when the interval between feedings increases and the infant sleeps through the night or when an illness prevents normal feeding routine. If the blood sugar falls to a low enough point, some patients may experience seizures. \n\nSince Type I patients are able to store glucose as glycogen but not release it normally, with time the stored glycogen builds up in the liver. Hormones, lactic acid, triglycerides, and other products are increased in the blood as the body attempts to raise blood sugar. Fats are stored in the liver along with the glycogen, which leads to enlargement of the liver. The liver does its many other functions normally, and there is not usually any evidence of liver failure. The kidneys are also enlarged due to glycogen accumulation. \n\nThe continued presence of low blood sugar eventually leads the body to experience severe biochemical abnormalities and delayed growth and development. Untreated patients may have muscle wasting and a buildup of body fat.\n\nWhen blood studies are done, it is discovered that there is usually a low blood sugar, elevated blood lactic acid, elevated cholesterol and other fats, and elevated uric acid concentration. High blood pressure has also been seen in a number of patients and when this occurs, appropriate treatment must be given.\n\nIn addition to the problems described above, patients with Glycogen Storage Disease Type Ib can develop frequent bacterial and fungal infections, due to abnormal functioning of the white blood cells. They may also develop chronic pancreatitis, chronic inflammatory bowel disease, and Crohn's disease. \n\nThe diagnosis of Type I GSD will always include blood studies, x-rays (including some of the kidneys), measurements, and ultrasound of the liver. Gene-based mutation analysis can be used to diagnose the majority of Type I patients, while liver biopsy analysis may be needed in some cases. \n\nThe treatments of Type I Glycogen Storage Disease are aimed at correcting the biochemical abnormalities and promoting growth and development. Current treatments consist of providing a continuous source of glucose by giving the patient glucose drinks frequently during the day and, in most cases, continuously overnight. Many medical centers have replaced these glucose feedings with uncooked cornstarch doses, mixed in water, Kool-Aid, or formula. \n\nLinks:\nvon Gierke Disease info from National Organization for Rare Disorders            [NORD]\nOMIM GSD Type I on Online Mendelian Inheritance in Man\n     searchable database\nGSD Type I from emedicine\nAmerican Liver Foundation information on Type I\nvon Gierke D
131452
I think that you should at least do some investigations to find out why your ALT is elevated. Do you know what your bilirubin, GGT, and alkaline phosphatase levels were?
118032
I had this problem also.  I ended up going to an endocrinologist for an unrelated problem.  I mentioned it when he said, "Do you have any other questions?"  He determined that I had vaginal and gastro-intestinal yeast.  He prescribed a drug called Diflucan that you normally take for a vaginal yeast infection.   His reasoning was that if you get rid of the yeast in that entire area, it is more effecacious.  I took one pill a day for an entire year, getting  blood testing every three months to make sure it wasn't damaging my liver.  I haven't had the problem since I stopped the medication in 1990, and my liver is fine.  If you don't want to seek the services of a physician, the advice given above about limiting your sugar, and intake of fermented foods is also a good way to control it, but doesn't completely stop the overgrowth of yeast in the body.
367726
Normal metabolism produces Ammonia within the body, which is toxic.  This Ammonia must be neutralized.  One of the ways the human body does this is the production of urea or uric acid in the liver.  Excess amino acids are also turned into Urea within the body.\n\nIf an excess of Uric acid occurs in the body ( Eating the wrong foods, kidney malfunction ), a condition called GOUT occurs...VERY painful joints and cartilage...
602188
There are liver enzymes (Cytochrome P450 oxidase) that detoxify our organism.\nSome people have low leavels of those enzymes and are prone to bigger toxicity.
562267
Please check out this site.  There is a wealth of information on it.  http://www.curezone.com/cleanse/liver/
985951
Takes some time for liver enzymes to elevate, could be several months to years. Hep.C. is transmitted via blood. Good time to use condoms :-)
873763
Probably a Magnesium deficiency.  \n\nMg is found in fresh vegetables - especially the green leafy ones - and almonds are a particularly good source.  It is excreted more if you are on diuretics, including caffeine, alcohol.  Magnesium supplements are good to get your levels up.
41633
SGOT stands for serum glutamic oxaloacetic transaminase. It is sometimes also abbreviated as AST (for aspartate transaminase). It is one of the blood enzymes that can be found in the liver, muscles, and blood, so if these are damaged, they leak out into the blood circulation so the amount of SGOT rises. Unfortunately, it is not very specific to any particular body part/system (because it could be due to a problem with your liver, or muscles, or blood), so if your SGOT is high, look for other enzymes (e.g. the SGPT) to help hone in on the precise cause.
92266
High levels of GGT on its own can sometimes simply be a reflection of heavy (alcohol) drinking. An anti-seizure medication such as phenytoin can also cause high GGT. If there is associated high ALT or AST, then liver disease is more likely.
1146816
Elevated liver enzymes are a direct result of hepatic (liver) cell destruction. This could be caused by many different things including hepatitis, cirrhosis, obstructions, and cancer. To name a few, of course there are others. Your physician would be able to identify which enzymes are elevated. There are several different enzymes which are tested (ask you MD). This question is hard to answer because it depends on what your diagnosis is. For instance if you have acute hepatitis, then no your enzymes would not decrease. It really depends on what the cause is. I wish you luck. :) Think positive!\n\n\n*** Just an FYI: secondary to the next person's response. A nephrologist studies Kidneys, not the liver. I would go to either your primary care doctor or a GI specialist, not a nephrologist.
653437
High levels of glucose are usually caused by uncontrolled  diabetes mellitus, pregnancy, excessive stress, renal tubular damage and brain damage\n\nHigh ketone levels indicate cold exposure, diabetes mellitus, dietary imbalances other metabolic problems-  So, you can eliminate those as possibilities.\n\nHemoglobin in the urine comnes from excess levels of free hemoglobin in the blood due to excessive red blood cell lysis-which can be caused by a blood disease, renal damage, or the normal mestrual bleeding, or possibly bladder infection.\n\nHigh levels of blood protein in the urine is the primary  indicator of glomerular damage. Other things that can cause this are excessive exercise (which can result in massive muscle breakdown-but these are not albumin), cold exposure and acute abdominal diseases-but the latter.\n\nLooks like renal damage-glomerular breakdown allowing proteins to pass through to the urine.