Tests of liver function

Liver function tests (LFTs or LFs), which include liver enzymes, are groups of clinical biochemistry laboratory blood assays designed to give information about the state of a patient's liver. Normally, only very small amounts of these enzymes are present in your blood. However, a laboratory report of elevated liver enzymes is not uncommon. Further, it is not unusual to see liver enzymes elevate while on the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. even if liver disease was not previously suspected because temporary immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. is unavoidable as a part of recovery.

Commonly ordered tests

Tests of liver function include:

  • albumin (Alb) – This protein is made specifically by the liver, and is the main constituent of total protein. Albumin levels are decreased in chronic liver disease such as cirrhosis. It is also decreased in nephrotic syndrome, where it is lost through the urine. Poor nutrition or states of protein catabolism may also lead to low levels. The half-life of albumin is approximately 20 days. Albumin is not considered to be an especially useful marker of liver synthetic function; coagulation factors are much more sensitive.
  • alanine transaminase (ALT) – Also called Serum Glutamic Pyruvate Transaminase (SGPT) or Alanine aminotransferase (ALAT), ALT is an enzyme present in hepatocytes (liver cells). When a cell is damaged, it leaks this enzyme into the blood, where it is measured. ALT rises dramatically in acute liver damage, such as viral hepatitis or acetaminophen overdose.
  • aspartate transaminase (AST) – Also called Serum Glutamic Oxaloacetic Transaminase (SGOT) or aspartate aminotransferase (ASAT), AST is similar to ALT in that it is another enzyme associated with liver parenchymal cells. It is raised in acute liver damage, but is also present in red blood cells, and cardiac and skeletal muscle and is therefore not specific to the liver.
  • alkaline phosphatase (ALP) – ALP is an enzyme in the cells lining the biliary ducts of the liver. ALP levels in plasma will rise with large bile duct obstruction, intrahepatic cholestasis or infiltrative diseases of the liver. ALP is also present in bone and placental tissue, so it is higher in growing children (as their bones are being remodelled) and elderly patients with Paget's disease.
  • total bilirubin (TBIL) – Bilirubin is a breakdown product of heme (a part of haemoglobin in red blood cells).
  • gamma glutamyl transpeptidase (GGT) – Although reasonably specific to the liver and a more sensitive marker for cholestatic (condition where bile cannot flow from the liver to the duodenum) damage than ALP, GGT may be elevated with even minor, sub-clinical levels of liver dysfunction. It can also be helpful in identifying the cause of an isolated elevation in ALP. GGT is raised in alcohol toxicity chronic).

Interpreting liver function levels that are out of range

Abnormal liver function measures are expected to be seen in many MP patients because these measures are an indication of an inflammatory response to infection. The experience of Autoimmunity Research FoundationNon-profit foundation dedicated to exploring a pathogenesis and therapy for chronic disease. has, thus far, shows that as long as immunopathology is tolerable while liver function remains abnormal, there's no need to make any changes in dosing of the MP medications. However, physicians and patients should always assess if immunopathology is too strong. If this is the case, taking measures to reduce immunopathology is always recommended.

Note that NSAIDs (non-steroidal anti-inflammatory drugs) such as Tylenol can increase liver enzymes. If pain medication is needed, an alternative should be considered. Nutritional and herbal supplements may also affect values of liver function.

Beneficial effects of olmesartan on liver disease

The renin-angiotensin system (RAS) is frequently activated in patients with chronic liver diseases. Angiotensin-II (AT-II) has been suggested to play an important role in the progression of liver fibrogenesis.1) 2)

Some of the documented protective effects of the angiotension receptor blocker, olmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. , include the ability to:

  • inhibit liver fibrosis and aid liver healingOlmesartan medoxomil was given to fibrotic rats. Liver hydroxyproline content, the mRNA expression of collagen alpha1(I) and alpha-smooth muscle actin (alpha-SMA), and plasma levels of transforming growth factor-beta1 (TGF-beta1) were significantly reduced by olmesartan treatment, suggesting that olmesartan improved liver fibrosis.3) A second study came to similar conclusion.4)
  • reduce fatty liver – Fatty liver developed in Zucker fatty rats was ameliorated by olmesartan treatment.5) “Taken in sum,” one team concluded, “ARBA drug which is an angiotensin receptor blocker. One of the ARBs is olmesartan (Benicar). Not all ARBs activate the Vitamin D Receptor. improves the overproduction and accumulation of TG in the liver associated with insulin resistance, and it does so through mechanisms independent of its hypotensive action.”

Patients experiences

Prior to beginning the MP, most of my bloodwork results were skewed, including the liver enzymes. The cyst on my liver has remained stable, but the blood levels began to normalize within three to six months after beginning the Protocol.

Carole, MarshallProtocol.com

My liver function test was normal on 11/4/06 after being abnormal in 2004 and 2005. Documented.

Scooker48, Marshall Protocol.com

I also wanted to note that a couple of years ago independent of the MP I had a slightly elevated ALT reading. My doc wasn't too worried because he said typically it was a fairly high reading which caused medical concern but he had no clue why it was just slightly elevated. A couple of months later I decided to google it and found a newly released study from UNC-CH that Tylenol could raise ALT levels slightly even in healthy people. The weird thing was that it didn't take much and the elevation lasted several days after the Tylenol was stopped. I also found that environmental toxins and junk food could raise the values according to some sources.It just sounds like the ALT reading is very sensitive in some of us. Just think what a total bacterial dump would do to something this sensitive.

Mindy, MarshallProtocol.com

===== Notes and comments =====

Couldn't find a study to support this:

Cell death (apoptosis) elevates ALT and resolves fibrotic tissue

The sensitive enzyme ALT is elevated when there is liver inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. and cell death (apoptosis). We know that when the immune system is effectively fighting infection, the result is cell death. But this is the road to recovery.

This article about research funded by the Wellcome trust will help you understand that cell death precedes cessation of fibrosis. The article explains that fibrotic damage can/will break down after the liver has regenerated. This research is in line with Dr. Marshall's thinking about fibrotic tissue reversion.

Macrophages, one type of white blood cell, have the duty of killing invaders like bacteria. Macrophages are phagocytes, or “eating cells.” Macrophage are the “big eaters” of the immune system. Take a look at the video clip on this web source by clicking on “time-lapse movie” to see how a white blood cell engulfs an enemy. This is what happens to bacterial invaders.

But engulfing or “eating” the threatening pathogens doesn't finish the job. The macrophage has to die to kill the enemy. Otherwise, bacteria may be able to live and even replicate safely inside the macrophage and the human host will still be ill. This could be serious, considering that the life span of a macrophage may be months or even years. Even slowly-reproducing bacteria might establish a stronghold by living inside macrophages.

The MP supports the immune system macrophages that are holding bacteria they have eaten. Once the antibiotics weaken the intracellular bacteria, the immune system naturally kills them off, and in the process, the infected white blood cells die. Toxic chemicals spill into the host tissue and blood. The host suffers the effects of immunopathology by temporarily feeling worse, even though the cell death will result in better health now that the pathogen is dead.

ABC Australia has a three-part series in their “Great Moments in Science” called “Apoptosis” in this link. It explains the natural process of cell death for the greater good and health of the host.


===== References =====

Yoshiji H, Kuriyama S, Yoshii J, Ikenaka Y, Noguchi R, Nakatani T, Tsujinoue H, Fukui H. Angiotensin-II type 1 receptor interaction is a major regulator for liver fibrosis development in rats. Hepatology. 2001 Oct;34(4 Pt 1):745-50. doi: 10.1053/jhep.2001.28231.
[PMID: 11584371] [DOI: 10.1053/jhep.2001.28231]
Yoshiji H, Kuriyama S, Noguchi R, Ikenaka Y, Kitade M, Kaji K, Yoshii J, Yanase K, Yamazaki M, Asada K, Tsujimoto T, Akahane T, Uemura M, Fukui H. Angiotensin-II and vascular endothelial growth factor interaction plays an important role in rat liver fibrosis development. Hepatol Res. 2006 Oct;36(2):124-9. doi: 10.1016/j.hepres.2006.07.003. Epub 2006 Aug 17.
[PMID: 16919500] [DOI: 10.1016/j.hepres.2006.07.003]
Kurikawa N, Suga M, Kuroda S, Yamada K, Ishikawa H. An angiotensin II type 1 receptor antagonist, olmesartan medoxomil, improves experimental liver fibrosis by suppression of proliferation and collagen synthesis in activated hepatic stellate cells. Br J Pharmacol. 2003 Jul;139(6):1085-94. doi: 10.1038/sj.bjp.0705339.
[PMID: 12871826] [PMCID: 1573934] [DOI: 10.1038/sj.bjp.0705339]
Oakley F, Teoh V, Ching-A-Sue G, Bataller R, Colmenero J, Jonsson JR, Eliopoulos AG, Watson MR, Manas D, Mann DA. Angiotensin II activates I kappaB kinase phosphorylation of RelA at Ser 536 to promote myofibroblast survival and liver fibrosis. Gastroenterology. 2009 Jun;136(7):2334-2344.e1. doi: 10.1053/j.gastro.2009.02.081. Epub 2009 Mar 18.
[PMID: 19303015] [DOI: 10.1053/j.gastro.2009.02.081]
Syntax error [pubmed plugin]
home/tests/liver.txt · Last modified: 09.14.2022 by
© 2015, Autoimmunity Research Foundation. All Rights Reserved.